Order Diplomonidida

No mitochondrion, No Golgi, two nuclei.

Family Hexamitidea

1- Giardia lamblia (G. intestinalis)(Intestinal flagellate)

Host: Man, more common in children than in adults.Habitat: Upper part of small intestine especially the duodenum and gall bladder. Morphology : 1.Trophozoites:

Size: 10 – 18 micr. Shape: Pear-Shaped, a sucking disc is found on the ventral side of the anterior broad end that can be seen in lateral view. Flagella: 4 pairs, one is directed anteriorly, one posteriorly and the other two run alongside the body.Nucleus: 2 vesicular nuclei lying at the broad end (look like two eyes ).Axostyle: Slender and lying along the center of the body.

2.Cyst:Size: 10 x 8 micr. Shape: Oval. Nuclei: 4, lying at one pole.At the longitudinal axis of the cyst, the backward passing intracytoplasmic flagella form the "axoneme" (not true axostyle)Cytoplasm: Finely granular, fibrils and coma-shaped bodies can be noticed.

Mode of infection: Infection occurs by ingestion of the cyst stage (infective stage) with food or water Life cycle: Infection occurs by ingestion of the cyst stage (infective stage) with food or water. In the duodenum the cyst wall dissolves releasing the trophozoites, which attach to the mucosal wall.

Pathogenicity:

Subphylum MastigophoraSubphylum Mastigophora

Most infections are symptomless, or there is chronic diarrhoea, steatorrhea, dull epigastric pains and flatulence, poor appetite and loss of weight, cholicystitis may be present. It may interfere with absorption of fat, deficiency in fat soluble vitamins occur and the colour of stool is clay or greenish

Diagnosis: Finding cysts or trophozoites in the stool.

Treatment:Flagy1 (Metronidazole).

Giardia spp. of animals:

Giardia cati (cats), Giardia canis (dogs) and Giardia muris (Rats)Giardia caprae (goats), Giardia equi (equines)

Cyst stage of Gardia lamblia

Giardia lamblia cyst Giardia lamblia trophozoite

Life cycle of Giardia lamblia

2- Genus HexamitaHexamita meleagridis

Host: Turkeys.Habitat: Small intestine Similar to Giardia in life cycle and morphology with exceptions.Morphology:1. Trophozoite: 10x5 um, pyriform shape with 2 nuclei, 2 axostyles, and 6 anterior (divided into two groups of 3) and 2 posterior flagella.2. Cyst: oval with 2-4 nuclei. Pathogenesis:It causes infectious catarrhal enteritis which leads to foamy watery diarrhea, stunting, malnutrition, rapid loss of weight and death.Mode of infection: Contaminated food and water by trophozoites or cysts.

Trophozoite of Hexamita meleagridis

Order Trichomonadida        Family Monocercomonadidae

Genus Histomonas Histomonas meleagridis

Host: turkeys Chickens, and pheasants.Habitat: Caeca and liver.Disaese: Black head disease (Enterohepatitis)

Morphology:The parasite is polymorphic and its appearance depends upon its

location and the stage of the disease. The forms in the tissues have no discernible flagella, although there is a basal granule near the nucleus.

1. The flagellated stage:Occurs in the lumen of the caeca. The same form is found in culture. Its body is amoeboid. The endoplasm may contain bacteria, starch grains and other food particles. Nucleus: vesicular with a single dense karyosome, and it may contain as many as 8 scattered chromatin granules. There is typically a single short flagellum but as many as four may be present.There is no axostyle or undulating membrane which is characteristic for (Trichomonas).2. The invasive stage:It is an actively amoeboid stage with blunt rounded pseudopods. The cytoplasm is differentiated into an outer clear ectoplasm and an inner granular endoplasm. Particulates of food are found in the endoplasm, but no bacteria are observed.

3. The vegetative stage:It is found near the centre of the lesions (older lesions). It is larger and less active than the invasive stage.

4. The resistant stage:This stage is not a real cyst, but the individuals are packed together and seem to be enclosed within a dense membrane. They are extracellular, but they may be taken up by phagocytes or giant cells. This stage is more resistant than the other stages.

Life cycle:Reproduction is by binary fission. The naked trophozoites are delicate

and do not survive more than a few hours when passed with the faeces. Turkeys can be infected by ingesting trophozoites (infective stage). However, large numbers must be ingested to produce the disease. It was reported that transmission is through the eggs of the caecal worm (Heterakis gallinae). The parasites are carried inside the (Heterakis) egg. Eggs treated with disinfectants do not kill the parasite and thus are still infective. The Heterakis egg must hatch in order to transmit the protozoon. Histomonas has never been seen in infected eggs, but the results were taken from experimental infections with eggs. Some workers found the parasite in the intestinal wall of the worm and larvae.The possibility that arthropods may transmit (Histomonas) has been considered by a number of authors.

Pathogenesis:

Turkeys are most susceptible between 3 and 12 weeks of age. Chickens are less likely to be infected by Histomonas meleagridis.

When the parasite is released in the caecum, it enters the wall where it multiplies causing a characteristic lesion and one or both caeca are affected. The cecum is enlarged and inflamed. Perforations of the cecum and peritonitis can occur.

Later on the parasites pass to the liver through the blood stream. Causing infectious enterohepatitis or histomoniasis. Liver lesions will have white and green areas of necrosis.

Symptoms of infected birds are droopiness, ruffled feathers, yellowish diarrhea, hanging wings and tails.

The disease is commonly called blackhead because infections sometimes cause a bluish or blackish appearance of the skin of the head in some birds due to an excessive concentration of reduced hemoglobin in the blood or cyanosis or caused by secondary bacterial infections.

This disease is one of the important causes of death in turkeys and chickens all over the world.

Immunity:

Birds that survive infection are immune for life .In addition susceptibility decreases with age.

Diagnosis:Lesions in the caeca can be distinguished from those caused by

coccidia by microscopic examination of scrapings from the mucosa by finding parasite stage.Lesions in the liver should be differentiated from other similar lesions and in case of doubt, histology is helpful.

Control: Turkeys should be kept separate from chickens, since the latter are

carriers. Young turkeys should be kept separate from adults. Care of shoes and utensils as they may transmit the infection from

flock to another. Droppings of birds should be removed regularly.

Treatment: Birds should be treated with Phenothiazine to kill the caecal worms,

but it is ineffective in controlling active outbreaks. Phenothiazine kills the worms but do not prevent their eggs from

hatching and releasing the parasite.

Trophozoite stage (A) Without flagella (B) With flagella

BA

Life cycle of Histomonas meleagridis

Family Trichomonadidae

There are several genera according to the total number of anterior flagellae:

1. Genus (Ditrichomonas).2. Genus (Tritrichomonas).

3. Genus (TetraTrichomonas). 4. Genus (Pentatrichomonas).

(Tritrichomonas faetus) infects cattle, horse and possibly pig. (Trichomonas vaginalis), (Trichomonas tenax and Pentatrichomonas hominis) infect man.

Genus Tritrichomonas(3 anterior flagella)

1- Tritrichomonas faetus(Urogenital flagellate)

Synonyms: (Trichomonas bovis), (Trichomonas genitalis)

Host: Bulls are the primary reservoir of the organism. Bulls are permanent

carriers and sources of infection. Habitat: The organism lives in the crypts on the mucosal surface of the penis and prepuce of the bull. In cows the parasite invades the vagina and uterus.

Morphology of Trophozoite:Shape: Pear-shaped or ovoid. Size: 10-26 um long by 3 to 15 um wide.Nucleus: Vesicular with a central karyosome, it lies at the anterior broad end.Flagella: 3 anterior and one posterior, the latter has free portion.Undulating membrane: Run all along the whole length of the body.

Costa: Prominent. Axostyle: Rod like, well developed and emerge from the posterior end of the body trough chromatic ring.

Transmission:By coitus and artificial insemination with infected material.

Pathogenesis and life cycle: After infection of cow, the parasite multiplies at first in the vagina

causing vaginitis. After 14-18 days they invade the uterus through the cervix, where they

produce low grade endometritis. They may disappear from the vagina or may remain there producing

low-grade inflammation and catarrh. Early abortion usually occurs 1-16 weeks after breeding, rarely abortion

occurs after 6 months gestation. If the placenta and faetal membranes are completely eliminated following abortion, the animal usually recovers spontaneously. Most cows self-cure after which developing immunity, although reinfections may occur. This is the most common course.

In Bulls: Commonest site of infection is the preputial cavity, although the testes, epididymis and seminal vesicles may sometimes be involved. There are no clinical signs once infection is established

Bulls remain permanently infected .Infected Bulls are regarded as permanent source of infection.

Diagnosis:The only sure method for diagnosing infection is to demonstrate the trophozoite stage microscopically either directly or in culture.

Treatment and Control: Infected bulls should be slaughtered. Proper management of bulls used for artificial insemination is especially

important, since they may spread the infection widely. Bulls should be examined for (T. foetus) before purchase, and the herds

from which they originated should be studied at the same time. Freezing the semen in the presence of glycerol cannot be expected to kill the parasite.

2-Tritrichomonas suis of pigsHost: pigs.

Habitat: In the nasal cavity, stomach, caceum, colon and occasionally small intestine.No disease is produced.

Genus Tetratrichomonas (Anterior 4 flagellae)

1- Tetratrichomonas gallinaeHost: Pigeons, Turkey and chicken are occasionally infected.Habitat: it infects the upper intestinal tract. Pathogenesis& clinical picture: It causes yellow, necrotic lesions in their mouth, oesophagus and crop of pigeon squabs and is frequently fatal. Infection is acquired via regurgitated crop contents from adult birds, which, although immune, remain carriers. Turkeys and chickens may occasionally become infected. Treatment: Dimetrinidazol is recommended for treatment.Control: depends on preventing access of wild pigeons to drinking water.

2- Tetratrichomonas gallinarum

Host: (chickens and turkeys)Habitat: lives in the lower intestine of birdsPathogenesis: producing diarrhoea, loss of appetite and loss of weight. It could be treated with 2-amino-5-nitrothiazole.

3- Trichomonas vaginalis

(Human urogenital flagellate)

Trichomonas vaginalis is a common and host-specific pathogen of women vagina and male urethra. Like T. foetus, it is venereally transmitted and the clinical signs of inflammation are largely confined to females.

Trichomonas featus

T. vaginalis

T. gallinae

Order KinetoplastidaFamily Trypanosomatidae

(Haemoflagellates)

Some common features of these parasites are:1. All members of the family have similar life cycle. They require insect

vector as intermediate host.2. Parasites metamorphose during development. The number of

developmental stages and tissue tropism are different for each species.3. They live in blood and tissues of their vertebrate host and in the gut of

their vector.4. No sexual cycle is known, multiplication is by binary fission.

Haemoflagellates exist in two or more of morphological stages.

Includes two important genera:1. Genus Leishmania.2. Genus Trypanosoma

1. Genus Leishmania

Members of this genus are parasite of man, dogs and rodents. They are obligate intracellular parasites. Have heteroxenous life cycle. Endemic in 88 countries on five continents, 12 million people are infected.

They occur in two forms:1- Leishmania (Amastigote form) in the definitive host.2- Leptomonad( promastigote form) in the culture or in the gut of the

vector.Vectors: Members of family Psychodidae Phlebotomus sp. Old World sp. and Lutzomyia New world sp.

There are three species of veterinary importance (occur in dogs), causing 3

clinical syndromes

1. Visceral LeishmaniasisLeishmania donovani

2. Cutaneous LeishmaniasisLeishmania tropica

3. Mucocutaneous LeishmaniasisLeishmania brazieliensis

Life cycle:

When the female sand fly bites an infected person with Leishmania sp it takes the organisms (Leishmania bodies) with the blood meal.

Within the blood meal, Leishmania bodies (amastigote) form change to Leptomonad (promastigote) form.

The promastigotes multiply (binary division) while attaching to the gut epithelium.

Forward migration of the parasites to the esophagus and proboscis. (Salivary glands are not infected).

Obstruction of the esophagus take place .When the sand fly bites a healthy person it regurgitates the infective stage (leptomonad form) in the biting site where inoculation of the infective stage take place.

In the vertebrate host, leptomonad (promastigotes) forms are phagocytozed by host macrophages. Transform into amastigotes, and multiply by binary fission .The amastigotes form break the infected cells and re-infect other cells (reticulo-endothelial cells) and ready to repeat its life cycle.

If ingested by feeding sandflies (female), amastigotes transform back into promastigotes, which require at least 7 days becoming infective.

At the biting site, initially there is a small papule.

In case of the L. tropica, the parasites produce Cutaneous leishmaniasis, usually a self-healing lesion called "oriental sore". The reaction is confined to the skin, thus the parasites do not circulate in the blood to the internal organs.

Whereas in L. donovani, the parasites migrate to endothelial cells of the reticuloendothelial system and polymorphonuclear leukocytes of the blood, spleen, lymph and bone marrow, and produce visceral leishmaniasis, which can be fatal if untreated.

In the mucocutaneous leishmaniasis initiates with as cutaneous lesion at the biting site but the parasites can undergo metastasis to the nose and mouth and cause a disfiguring and untreatable disease.

1. Leishmania donovaniHost: Man and dogs.

Vector: Phlebotomus papatasii (sand fly)Disease: The cause of fever called Kala- azar, dumdum fever, black fever or visceral leishmaniasis.

Geog. Distribution: India, Sudan and Middle East. Transmission:

The organisms can be transmitted not only by sand flies but also congenitally and parenterally (e.g., through blood transfusions or sharing of needles).

Clinical picture and pathogenesis:

I) In man: Chronic disease with irregular fever lasts for several weeks or months

with characteristic double crises. Hepatosplenomegaly without ascitis is one of the characteristics to

differentiate Kala-Azar from Bilharziasis. There is also anemia, leucopenia with eosinophilia.

Thrombocytopenia is another characteristic feature of the disease (due to invasion and multiplication of the parasite in the R.E.C. of bone marrow).

There is also post-cutanous stage called Post Kala-Azar dermal leishmaniasis.

II) In Dogs:Visceral form is more common develop 'spectacles' (like wearing glasses) due to depilation of the hair around the eyes, followed by loss of body hair and eczema.Irregular fever, aneamia, cachexia and generalized lymphadenophathy are typical signs.

Diagnosis: Clinical picture. Smear from spleen pulp, sternal puncture, and liver biopsy or from the

blood to be fixed in methanol, stained with Giemsa stain and examined for intracellular amastigote form.

Animal inoculation with the suspected material into Golden hamester in order to isolate the parasite after a few weeks from its viscera.

Cultivation on N.N.N. (Nicolle, Novy and Mac Neal) composed of: Agar, Sodium Chloride, distilled water and defibrinated rabbit’s

blood. The leptomonad forms are detected and take a "rosette- shape ".

Serological diagnosis: Indirect haemagglutination test, ELISA. Formol- ge1 (Napir aldhyde test); One c.c. serum of the suspected patient is added to one drop of 40% formalin, if white jellification occurs within ½ hour it is considered as positive.

2.Leishmania tropica

Host: Man, (dogs and rodents are reservoir hosts). Vector: Phlebotomus papatasiiDisease: The cause of Oriental sore, Aleppo boil, Bagdad’s boil or Delhi sore. Gego. dist.: It is present where the vector or sand fly is present, especially Egypt, Iraq, Syria, India, Iran.

Pathogenesis :( Dogs have similar clinical picture as man)1- Nodules: In the skin where sand fly bites (face, arms and legs), of about

2 cms in diameter. The nodules become changed into vesicles.2- Vesicles: Hot, red and swollen. When the vesicle bursts, it forms ulcers.3- Ulcers with raised edges. Contact with infected persons may give the

disease (Leishmania bodies is infective stage).4- Healing results in a disfigured scar tissue.

Diagnosis: Clinical symptoms. Smear form aspirated material taken from the red zone of the ulcer

stained with Giemsa stain and examined for amastigote form. Culture on N.N.N. Where the leptomonad forms take rosette- shape. Inoculation of laboratory animals (golden hamster), to isolate the

parasite after a few weeks

Treatment of Leishmaniasis: Antimony preparations (berberine sulphate).

Immunization: By using the native method, the Leishmania bodies are collected from patient carrying ulcers to be used as vaccination in the back of children covered with plaster- bandage.

Life cycle of Leishmania Spp.