Histomonas meleagridis disease is a kind of infectious disease which is transmitted by eggs or larvae of the bacterium Heterakis gallinarum, this disease mainly affects chickens and turkeys. In the following article we will learn more about this very common pathology and we will know which are the necessary cares to treat it.
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Histomonas meleagridis
Histomonas meleagridis is a unicellular flagellentragender which has an amoeboid form and as a parasite, especially in chickens and in turkeys, but also a variety of other birds, infects. In these birds, the parasite can cause a very infectious intestinal disease called histomoniasis, also known as shin disease.
Especially in turkeys, this is often fatal. After infection, the pathogen is mainly found in the lumen of the cecum and in the liver parenchyma, where the parasites are extensive and cause necrosis.
The exact route of transmission is not yet fully elucidated. Some studies even reported transmission by the eggs of the nematode Heterakis gallinarum, itself a parasite. Other authors reported a possible cyst stage.
It causes a type of infectious enterohepatitis or histomoniasis which is a black head disease. Histomonas meleagridis can infect many birds, but is most deadly in turkeys. It inhabits the lumen of the cecum and liver parenchyma, where it causes extensive necrosis. This disease is transmitted by another cecal parasite, called the nematode Heterakis gallinarum.
Etiology
Histomonas meleagridis is transmitted in most cases by the embryonated eggs of Heterakis gallinarum, a cecal nematode, but in certain cases it is transmitted by direct contact with infected birds. The larvae of histomonas gallinarum are found in 3 species of earthworms, and most birds become infected by consuming these worms.
Earthworms tend to eat the infected eggs of the nematodes, which can remain dormant in the soil for many years. Within days of ingestion, histomonas meleagridis is released from the Heterakis nematode larvae into the bird’s intestine and is where it begins to rapidly replicate in the cecal tissues.
It then migrates to the submucosa and muscle mucosa causing serious and severe necrosis. The parasite passes to the liver via the circulatory system or the peritoneal cavity, where it causes further necrotic lesions. Histomonads interacts with other organisms present in the digestive system, such as bacteria and coccidia, depending on them for full virulence.
Description
Histomonas meleagridis is a microscopic, pleomorphic protozoan particle, and can exist in two forms, the amoeboid and the flagellate. Within the tissue, it is present as an amoeboid protozoan, while in the lumen or free in the contents of the cecum, it inhabits as an elongated flagellated form.
The amoeboid form is typically about 8 to 15 mm in diameter, while the flagellated form can reach up to 30 mm in diameter. Histomonas meleagridis do not possess mitochondria, but produce energy within hydrogenosomes. The flagellum shows the common type called 9 x 2 + 2.
Life cycle
Histomonas meleagridis reproduces by binary fission. The free trophozoites are very delicate and can survive only a few hours in the external environment.
However, when transmitted between flocks in the eggs of Heterakis gallinarum, a cecal nematode, which in turn can be transmitted by worms that ingested the nematode eggs , gain entry into the nematode eggs.
The eggs with the trophozoites are transmitted to the environment through the feces. In this way, the trophozoitescan remain viable for up to two years in the external environment.
Within turkey flocks, histomonas meleagridis is also known to be transmitted directly from bird to bird. Histomonads are either released from heterakid nematode larvae in the ceca or after direct infection through the cloaca, and replicate rapidly in cecal tissues.
They migrate to the submucosa and muscularis mucosae and cause severe necrosis. The parasites then move to the liver through the vascular system. There, they cause a typical crater necrotic lesion. Mortality in turkey flocks can be very high at an average of 80 to 100%.
Pathogenicity
Histomonas meleagridis is the causative organism of histomoniasis in poultry. It induces extensive and very severe necrosis of the mucosal and submucosal tissues of the cecum and liver parenchyma. The lesions are sometimes exacerbated by other pathogens such as Escherichia coli and coccidia.
Symptoms usually appear within 7 to 12 days after infection and include a sort of:
- Depression
- Decreased appetite
- Impaired growth
- Increased thirst
- Sulfur-yellow diarrhea
- Apathy
- Drooping wings
- Unkempt feathers
Symptoms are highly fatal to turkeys, but cause less damage in chickens. However, in broiler outbreaks can result in high morbidity, moderate mortality and extensive culling, leading to poor overall flock performance.
The concurrence of Salmonella typhmurium and E. coli was found to cause high mortality in broilers. Birds that are young, particularly those between 3 and 12 weeks of age, are the most susceptible to these diseases. In general, symptoms are profound in turkeys, while chickens are usually asymptomatic.
Diagnosis can be easily made by necropsy of the fresh or preserved carcass, particularly the liver. Recently, paromomycin has been approved by the Italian authorities for its treatment. However, good farm management and sanitation are the essential effective strategies to control the spread of infection.
Diagnosis and Control
Diagnosis can be easily made by necropsy of the fresh or preserved carcass, particularly the liver. Recently, paromomycin has been approved by the Italian authorities for its treatment.
However, good farm management and sanitation are the essential effective strategies to control the spread of infection.
Histomonosis is a protozoan disease caused by histomonas meleagridis , and characterized by necrotic lesions affecting the liver and cecum. Clinically, sulfuric yellow stool and depression are observed. A very characteristic presentation is the blackening of the skin of the head, i.e. the head turns black due to cyanosis.
Diagnosis
From the anatomopathological point of view, a kind of bilateral enlargement of the cecum with thickening of its walls is observed. The etiologic agent is histomonas meleagridis, a polymorphic flagellate that is present as a flagellate in the cecum and as an amoeba in the tissues.
Trophozoites survive for several hours in the environment, but in Heterakis eggs, they remain inactive for more than 1 year. Frequently, the presentation of typhlitis is the cause of adhesive peritonitis.
The species most at risk are turkeys, chickens, pheasant, rock partridges, guinea fowl and geese. In particular, turkeys are the most susceptible species between 3 and 12 weeks of age and chickens between 4 and 6 weeks of age.
The cecal mucosa is usually ulcerated. The main vector is Heterakis gallinarum via eggs and larvae, where they are found in histomonas meleagridis forms. In some of the wild birds may also serve as vectors. The cecal contents are often mixed with blood.
In old cases, crusts of dense caseous masses form within the cecum, which thicken the intestinal wall and tend to reduce the lumen which is the upper right part in cross section through the cecum.
Worms are mechanical vectors of H. gallinarum larvae. The main reservoirs of infection are hens and chickens. The morbidity rate reaches 90 % and the mortality rate is 70 %.
In the liver, delimited coagulative necrosis of various sizes and colors can be observed. Invasion united with Heterakis gallinarum and Ascaridia galli.
Necrosis is frequently observed as yellowish to gray or red foci that are like a kind of hemorrhagic infarcts which are well delineated with a diameter of about 1 to 2 cm.
Studies performed on the birds
The spread of histomonas meleagridis infections by groups of turkeys in the absence of the cecal worm vector Heterakis gallinarum was studied in a battery cell model. Battery-reared chickens were exposed at 2 weeks of age by mixing with infected birds in cages that had paper-lined floors.
One treatment received no exposure, while other birds were mixed with 2, 3 or 4 caged birds which were inoculated by cloaca with cultured histomonas meleagridis.
The inoculated birds died between 7 and 13 days post inoculation (DPI) and showed some hepatic and cecal lesions typical of histomoniasis. By 14 DPI, 87.5 % of the directly inoculated birds died or had severe histomoniasis lesions. Turkeys mixed with 2, 3 or 4 infected birds were infected at a rate of 72 %, 80 % or 75 %, respectively.
In another experiment conducted, 2 cage birds i.e. 25 % of them were inoculated with histomonas meleagridis from the culture and allowed to mix with other bird species for 1, 2, 3 or 4 days.
2 out of 12 of the birds i.e. 16.7 % of the birds had minor cecal lesions after contact with inoculated birds for 1 day, but 87.5 % to 100% of them were infected if the inoculated birds remained in the cage for 2 or 4 days.
Contemporaneous inoculation with the cecal coccidia called Eimeria adenoeides as a kind of predisposing factor in blackhead infections was studied using the model.
Turkey turkeys directly inoculated with histomonas meleagridis were allowed to mix for 5 days with uninoculated birds that had received inoculation with 0, 10 (3) or 10 (4) sporulated ocysts.
Coccidian infection appeared to interfere with the transmission of shin infection in 7 IPD, as suggested by decreased severity of cecal lesions and a lower percentage of infected birds.
How to transmit
The disease caused by histomonas meleagridis is commonly known as shiners and was first described in turkeys in 1895.When it was determined that a milder form occurred in chickens that became carriers, poultry producers stopped raising turkeys on land previously used for chickens.
Chicken cecal worm, Heterakis gallinarum and earthworms are accessory hosts. Turkeys become infected by eating infected Heterakis eggs or worms containing juvenile heterakids.
Direct transmission through feces is uncommon due to the low survivability of histomonads when not protected by Heterakis eggs.
Losses are greatest in turkeys (especially under 3 months of age) but Histomonascan infect chickens, pheasants, chukars, grouse, peacocks, guinea fowl, quail and pheasants. The natural incubation period is 7 to 12 days and mortality in turkeys can approach 100% and morbidity is 80% to 90%.
Recovered birds may continue to harbor histomonads in their ceca. Affected turkeys have sulfur-colored feces; depressed, drooping wings; and a stiff gait. Although the disease is called shiners, not all turkeys will have a cyanotic head.
Chickens often have an unapparent infection without sulfur-colored feces but may have blood in the feces. Leukocytosis, decreased uric acid and hemoglobin, transient increase in blood sugar, and increased aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) are usually observed.
Macroscopic lesions are mainly found in the cecum and liver. Lesions in the cecum include enlargement, thickened hyperemic walls, caseous luminal cores, and mucosal ulceration.
Lesions in the liver commonly have circular, depressed areas of necrosis circumscribed by a raised ring (bull’s-eyes). Diagnosis is usually based on clinical signs and macroscopic lesions.
Demonstration of histomonads in freshly killed birds is difficult because histomonads die quickly and are more difficult to identify. The best prevention is not to place turkeys in ranges previously inhabited by chickens or other game birds and to control worms. Rotation of ranges is not practical, as histomonads
Medical Treatment
Garlic essential oil can be an effective preventive or curative treatment against various flagellated poultry parasites. Allium sativum bulbs were investigated in vitro on Tetratrichomonas gallinarum and histomonas meleagridis ; the main active ingredients were dialysulfide and disulfide (79 %).
It appears that these oils may be useful as therapeutic agents against various poultry parasites described by Zenner in 2003.
Three battery tests were performed to study the anticrypto-spidial efficacy of diclazuril and toltrazuril, together with a garlic extract. The efficacy of the garlic extract was 24.4 %. It was concluded that garlic oil cannot be recommended for prophylaxis or treatment of cryptosporidiosis in chickens.
The Antimicrobial
The antimicrobial potential of various Harmala seed extracts has been investigated in vitro on multiple antibiotic resistant pathogens (19 bacteria) and some selected protozoa ( Histomonas meleagridis , Tetratrichomonas gallinarum and Blastocystis sp .)
Poultry isolates. Harmala seed extract was found to inhibit the growth of all bacteria and protozoa. The potential role of the four known ß-carboline alkaloids in crude harmala extracts was also investigated for their antimicrobial activity.
The activity of the pure alkaloids was in the order harmane > harmaline > harmalol > or = Harmine for all bacteria, whereas for protozoa, it was different depending on the microorganism. It is concluded that harmala or its alkaloids could probably be used for the control of antibiotic resistant bacterial isolates as well as protozoa.
History and possible Antihistomonals
Histomonosis (shinbone) is a disease of galliform birds caused by the flagellate protozoan histomonas meleagridis. Its main organs are the cecum and liver. Especially in turkeys, mortality can be very high up to 100%. In the 60’s and 70’s several antihistomone compounds were found which are effective as nitarsone and dimetridazole developed and the disease was controlled.
After the use of these types of antihistomonals was banned in production animals due to possible toxic and carcinogenic properties, the disease reappeared again. The aim of the studies in this thesis was to optimize and develop methods for the detection and typing of histomonas meleagridis and to examine new possibilities to control the disease.
The culture of histomonas meleagridis was optimized by adding more than 100 mg instead of 12 mg of rice powder to the culture medium ( Dwyer medium ). This resulted in a yield that was 10-fold higher of parasites and the possibility of prolonging the cultures by the addition of rice powder.
It was also discovered that a complex component, chicken embryo extract, which was redundant.
Another constituent, horse serum, was found to be essential. Several new antihistomonal products were examined which were possible using in vitro models that were based on the culture produced and, if effective, in vivo.
Aromabioic ™ and tiamulin were not effective and were not tested further. Enteroguard ™ and Protophyt ™ had no antihistomonal effect in vivo. Paromomycin, however, protected turkeys against an otherwise lethal challenge with histomonas meleagridis ( full protection at 400 ppm and partial protection at 200 ppm ).
A blocking ELISA was developed for the detection of antibodies in chickens and turkeys.
The monoclonal antibody required for this assay was generated against proteins extracted from histomonas meleagridis using a detergent called Triton X – 114. While both chicken and turkeys were subsequently challenged with histomonas meleagridis, the ELISA showed no cross-reactivity with Tetratrichomonas gallinarum.
The ELISA is, for example, useful for seroepidemiological studies for the distribution of histomonas meleagridis in chickens, which are considered a reservoir for the parasite. Finally, a new subtyping technique (called C-profile) was developed. It is based on molecular techniques (PCR and sequencing).
The internal transcribed spacer 1 (ITS1) region of the rRNA gene was found to be sufficiently variable for subtyping. Three subtypes of histomonas meleagridis were found.
Type III is possibly Parahistomonas meleagridis, a nonpathogenic protozoan described a few decades ago. Subtyping is useful if different genotypes are associated with different pathotypes.
The C-profile was applied to a closely related human pathogen: Dientamoeba fragilis and was found to be a promising molecular epidemiological tool to study the transmission, geographic distribution and strain-pathogenicity relationships of this parasite.
Additions to the life cycle of histomonas meleagridis
Many researches throughout history provided concrete data that infections in turkey flocks occurred from the ingestion of embryonated eggs of the cecum worm called Heterakis gallinarum, or the ingestion of worms carrying the larvae of the cecum worm, these are the ones that have the highest level of altering the organism.}
This mechanism does not explain the phenomenon of the rapid spread of blackhead through a flock of turkeys, thus leading some experts to raise certain questions, which were based on intermediate hosts that might be involved.
Because of these opinions, some experiments were recently generated where turkeys from places like Turkey were placed in pens together with other turkeys inoculated directly, in the absence of any other possible carrier or host, in order to try to support their own theory.
The results found in this study were decisive, since they indicated that the non-inoculated birds easily contracted the infection, became sick and died. At the end of the study, for such reason all birds had died or were sick with blackheads as part of the result.
Where do turkeys get infected?
It is common for veterinarians and other researchers to be unable to find Heterakis worms associated with outbreaks in turkeys due to different analyses performed on these species in order to get the answer.
For this reason, it has been opportunely taken over time that all fattening reproductive farms are highly contaminated with cecal worm eggs (Heterakis gallinarum), which are the only known biological vector of the blackhead organism, and for this reason certain questions have arisen.
As for worms, it is believed that they can harbor cecal worms until they are eaten by chickens or turkeys, but this is only an “extra” reservoir of infection and not a necessary part of the worm’s life cycle. For this reason, farms remain infectious for turkeys for many years according to several studies.
Where did shinbone disease come from?
The first originating cases of shiners in turkeys were reported from Rhode Island in the year 1892. It is in some cases surprising that the common pheasant or also known as the Chinese ringneck was introduced into the United States in 1881, and quickly spread widely for release as a game bird.
Outbreaks of shiners declined in the turkey industry in the New England area, and followed farmers to the Midwest, and in this way reached different areas until they reached Canada and the Far West. Until World War II, shinbone was considered the leading cause of mortality in turkeys.
As for game birds in particular are not taken as a source of infection, but nevertheless could be another reservoir of infection as they may be present in areas where turkeys are raised and inhabit there without knowing if they can be infected.
How do you control shiners?
The prevention of blackhead in turkeys by management is twofold:
- prevention of exposure by quarantine or isolation, especially by avoiding any contact with chickens or game birds.
- use of migratory barriers to avoid mixing of infected birds with non-infected birds.
Interestingly, contagious spread of blackhead by direct bird contact is not as important in chickens as in turkeys. Therefore, it is likely that infections in chickens result only from ingestion of Heterakis ova.
In addition, farm owners should be aware of their workers’ hobbies and discourage keeping chickens, pheasants, chukars or fighting cocks.
