1. Protozoology

All QS - morphology, location, main species, geographical distribution, epizootology,. epidemiology, LC, Pathogenesis, and clinical signs, pathology, diagnosis, treatment and control of parasite. Protozoan - one cell parasites, intracellular/extracellular. These are microscopic one-celled organisms.

1.Trypanosomosis in humans

Trypanosomosis in humans - by protozoa of genus Trypanosoma.

Classification:

• Phylum: Euglenozoa, subphylum: kinetoplasta, class: Kinetoplastea, Order: Trypanosomatida, fam: trypanosomatidae

• Genus: trypanosoma + Leishmania

There are 2 major forms:

1. Human african Trypanosomosis (African sleeping sickness) - SALIVARIA

2. American trypanosomosis (Chagas disease/american sleeping sickness) - STERCORARIA

Human african trypanosomosis (HAT) - “African sleeping sickness) - Salivaria

Caused by T. brucei complex:

• T. Brucei Rhodesiense (East african type) - Zoonotic, humans are occassionally infected, as it circulates primarily bw. animals and tse tse fly. Causes acute form, giving asymptomatic disease in animals, but they are imp. reservoir hosts. First symptom within a few months or weeks. Develops rapidly and invades CNS.

• T. Brucei Gambiense (African type) - Causes chronic form, infected for months/years without major signs. The patient is already in advanced stage when CNS is affected.

FH: humans, cattle, pig, car. Zoonotic.

Location: EC, in plasma, lymph, cerebral fluid and organs of resp. system.

Vector: Tse tse fly (Glossina spp.) Cyclic transmission.

Geography: Sub-saharan Africa

LC: Vector takes a blood meal from infected FH → ingestion of infective trypomastigote → develops into Epimastigote in vector (fly) and multiplies by binary fission → Migrates to salivary glands and multiply → develops into trypomastigote and make the vector infectious → next time tse tse fly bites → injects the parasite into blood of FH → multiplies by binary fission in blood, lymph and spinal fluid.

Pathogenesis and Clinical signs - 3 phases:

1. Primary lesion: chancre at bite site 2-3 days after the bite - raised cutaneous infl. swelling

2. Parasitemia: parasite in bloodstream produce irregular fever, insomnia, erythema and itching. enlargement of LN “winterbottom`s sign”, invasion of bone marrow - anemia.

3. Invasion of CNS: meningitis, encephalitis, severe headache, lethargy, deep sleep → coma → death.

Animals show abortion, infertility, anemia, weight loss, fever.

Diagnosis: Direct demonstration of parasite - Wet mount, Giemsa stained thin or thick smears (low sensitivity) - chancre fluid, bone marrow, Blood, LN, CSF. These two species are morpho. indistinguishable.

• Concentration: HCT - hematocrit centrifugation technique.

• Serological tests are of limited value - like ELISA, PCR.

Treatment:

• Ru: Diminazene aceturate - therapy, isometamidium - long lasting efficacy 2-6 months. Camels, equine, dog: Melarsomine (Diminazene is toxic).

• Humans: Pentamidine, IM - in first stage. Nifurtimox, oral in 2nd stage. Fexinidazole in first and non-severe second stage. (gambiense). Rhodesiense - suramin - in first stage, Melarsoprol in 2nd stage.

Control and prevention: control of the principal reservoir of infection like livestock and wild. Reduction of vectors - destruction of the flies habitats or use insecticides, fly traps, male flies sterilized in lab (SK).

American trypanosomosis, also known as Chaga`s disease (stercoraria)

By T. cruzi

FH: human, car, rodents, opossum, amardillo - reservoirs. Zoonotic! Naturally infect up to 150 species.

Transmission: Triatoma (kissing bug, blood-sucking), rhodnius and panstrongylus genus. Cyclic transmission.

• contaminated food, blood transfusion and fetal transmission. Vector bite people in the face when they sleep.

Location: EC trypomastigotes are found in the blood. Intracellular amastigotes are found in the tissue. Epimastigotes are found in the intestine of vector. Metacyclic trypomastigotes in rectum of vector.

LC: vector takes a blood meal from infected FH → trypomastigotes ingested → epimastigotes in midgut of vector → multiplies → metacyclic trypomastigotes → hindgut → vector then takes a blood meal from host (passes the trypomastigotes in feces, enter bite wound) → amastigotes form in cells → multiply in tissues → trypomastigotes enters blood → migrate to new sites, lymphatics, CNS.

Pathogenesis and clinical signs:

Dogs up to 1 year: Acute infection is death. In surviving dogs we see hepato-splenomegaly, anemia, edema, ascites, cachexia, respiratory symptoms and fever. Acute phase is followed by a transitional period 8-36 months with no clinical signs. Progressive chronic form show myocarditis and destruction of ganglia cells.

Humans: acute phase is asymptomatic. Incubation period is 10-20 years. Serious pathological changes can occur, like damage of the tissue cells and ganglia of the autonomic NS.

3 phases of disease:

1. Acute phase: Active infection, 1-4 months of duration. Most are asymptomatic (children most likely to be symptomatic)

2. Indeterminate phase: 10-30 years of latency. Relatively asymptomatic with no detectable parasitemia. Seropositive.

3. Chronic phase: 10-30% of infected shows cardiomyopathy or megasyndromes, like visceromegaly (enlargement of internal organs, dilation of esophagus and food regurgitation, megacolon).

• Humans may have edema in eyelids (romagna sign), edema of the satelit lymph node - local reproduction of the parasite (chagoma). Visceromegaly - cardiomegaly, megacolon.

Diagnosis:

• Dogs: in acute stage, thin and thick blood smear, concentration techniques. In chronic stage, trypomastigotes are missing or rarely present. Alternative methods are PCR and ELISA but can cause cross reaction with Leishmania in dogs.

• Humans: acute phase, detect by blood. Chronic phase, detect by serological test.

Treatment:

Dogs: Chemotherapy in dogs is difficult. In acute cases, give benzidazole daily for 2m (does not prevent subsequent chronic cardiac disease), vector control by insecticides, blood transfusion.

Humans: acute stage: nifurtimox, benzidazole. While allopurinol and azole antifungal agents are experimental. Chronic stage: Treat symptoms.

2. Trypanosomosis in animals

Species: (Salivaria)

1. Nagana Disease (animal african trypanosomes), by T. congolense, T. vivax, T. brucei brucei

2. Surra disease - chronic by T. brucei evansi

3. Dourine disease - chronic, by T. brucei equiperdum

OBS! Nagana, dourine and surra have very similar CS.

• nagana - fever, anemia, ventral edema, paralysis, death

• Dourine - fever, anemia, Genital edema, plagues + skin erup., paralysis, Death

• Surra - fever, anemia, ventral edema, paralysis, Death

Surra and Dourine - listed by WOAH as notifiable.

1) Animal african trypanosomes - Nagana disease, chronic, Only in Africa.

• caused by:

  1. T. congolense

  2. T. vivax

  3. T. brucei brucei

FH: Bo, eq, pig, car, camel (wild african game). mainly affecting cattle.

Vector: Tse tse fly (glossina spp). cyclic transmission. Glossina flies are viviparous, lifespan 14 days. Females produce 8-12 larvae during their lifespan.

Location: blood vessels

LC: Vector takes a blood meal from infected FH → ingestion of infective trypomastigote → develops into epimastigote → and multiplies by binary fission → migrate to salivary glands and multiply → develops into trypomastigote and make the vector infections → next time tse tse fly bites, it will inject the parasite into blood of FH → multiplies by binary fission in blood, lymph and spinal fluid.

Pathogenesis and clinical signs:

• Disease occurs 7-10 days after infection, higher body temp., HR, and BR, continuous worsening of health, permanent loss of fitness, clearly sick, variable appetite

• in start stage, diarrhea can be present,

• anemic, lacrimation (incr. tear secretion), emaciation + death, somnolence.

• Typical: Eq: edema of abdomen, scrotum, paralysis of N. facialis, unclotted MM. Dog: pharyngitis, ulcerative stomatitis, edema (eyes, genitals), gastritis.

• Cattle: enlargd prescap. LN, progress. emaciation.

Diagnosis: Identification of parasite in the blood giemsa, hematological examination - micro hematocrit, sero tests - ELISA.

Treatment: (resistance) - isometamidium chloride (toxic for Eq + camel), melarsomine, diminazine.

Prevention by vector control and permanent monitoring.

(står sammen med african animal trypanosomosis nagana i lectures - soo)

2) Surra Disease - chronic, in Africa, latin-america

Caused by T. brucei evansi (different from T. brucei brucei - as this is cyclic + mainly affects livestock, while evansi is non-cyclic)

• Non-cyclic transmission (no parasite development inside vector). Mainly transmitted by vector sucking blood and iotrogenic (reuse of needle). BUT in dogs, it can be by contaminated meat/blood.

FH: eq, camel, dog, cattle, elephants

vector: Tabanidae (horse fly), vampire bats

Location: EC, in plasma, lymph, cerebral fluid

LC: Inside mammalian host → mulitiply by binary fission in trypomastigote form, in the blood, lymph fluid and spinal fluid.

Pathogenesis and clinical signs:

• Fever, progressive anemia, progressive weakness, weight loss, lower body edema, patchy hemorrhages in conjunctiva, vaginal mucosa etc.

• Locomotor disturbances, CNS disorders (Paralysis, paresis).

• Dogs: Rapid acute course, death within a week or month.

Diagnosis: blood smears, lymph node aspiration. Hematocrit. ELISA, PCR.

Treatment: Suramin + vector control.

3) Dourine disease (Equine trypanosomiasis) - chronic, often fatal.

By T. brucei Equiperdum.

FH: horse, equids

Location: free in MM, tissue, bloodstream, and cerebrospinal fluid.

Vector: NONE! Rarely, it can be carried by blood-sucking flies, even if only mechanically. Mare → foal by MM, milk.

Transmission: sexual by breeding

Geography: endemic in some african, asia and latin-american regions + middle east and eastern Europe.

LC: Binary fission in various tissues.

Pathogenesis and Clinical signs: Characterized by genital edema, neurological dysfunction, skin lesions (silver-dollar plaques) and death.

• First stage (genital): genital edema (vulva, mammary gl., inner thighs), mild vaginal discharge, low-grade fever, inappatence

• 2nd stage (Skin): urticarial skin plaques/silver dollar plaques/tholiac spots on ribs, flanks, neck.

• 3rd stage (neurological): muscle paralysis - starting in face, neck → then to limbs → all muscles, facial nerve paralysis, hyperalgesia (pressure over withers), weight loss → cachexia → death.

Diagnosis: Usually undetectable in blood. Rarely found in urethral/vaginal mucus washing or scraping.

Clinical signs supported by serology: ELISA, IFA, CFT

Treatment and control: in many countries, treatment is not allowed, not recommended as it can suppress clinical signs. (eq is still transporters)

• Melarsomine can be used

• Examine horses before breeding, quarantine and euthanasia of horses with clinical symptoms.

• EU: Control breeding, quarantine + eliminate infected.

3. Leishmaniosis (cutaneous, visceral, mucocutaneous).

Order: Trypanosomatida, Fam: Trypanosomatidae, Genus: trypanosoma, Leishmania. Has 53 species known to infect humans, only 13 are zoonotic and morphologically indistinguishable. Their differentiation is based on clinical picture of disease, host and vectors, and molecular characteristics.

Species:

1. Visceral: L.donovani, L. infantum

2. Cutaneus: L. tropica, major, aethiopica

3. Mucocutaneous: L. mexicana, brasiliensis

Morphology: Ovoid organisms. Rod-shaped kinetoplast and rudimentary flagellum.

Location: Found in macrophages, cells in skin, liver, spleen, bone marrow, lymph nodes and mucosa, may also be found in leukocytes.

FH: Dogs, humans, and rodents. Zoonotic.

Vector/IM: sandflies of genus Phlebotomus (old world, Europe) and Lutzomyia (new world)

• Cyclic transmission by vectors. Worldwide.

LC: Amastigotes in blood/MF → ingested by sandfly (female) → promastigote in gut of fly → binary fission → migrate to pharynx → transmits pormastigotes into vertebrate host by inoculation → phagocytosed by MF → reverses back into amastigotes and divides, burst of cell → amastigote can affect tissue cells.

• Amastigote stage - vertebrate host (FH). Promastigote stage - sandfly (IH).

Pathogenesis and clinical signs - Leishmaniosis in Dogs:

We can separate the dogs into 2 populations:

• susceptible: activation of Th2 cells, high prod. of non-specific Ab, lack of cell-mediated immunity, genetic factors.

• Resistants: Activation of Th1 cells, low level of specific Ab, efficient cell-mediated response. Factors related to parasite.

In endemic areas - 50% of dogs may be infected without clinical signs. Clinical leishmaniasis starts as a visceral form, ca. 90% of dogs present also cutaneous lesions.

• Visceral form - Chronic systemic disease:

  • Incubation: 1-3 months to several years, generalized lymphadenopathy, weight loss, anorexia, apathy, hepato-splenomegaly, hypoalbuminemia, renal failure with proteinuria, incr. urination and drinking.

• Cutaneous form - skin lesions (starts in the head)

  • alopecia, nodules, pustules, excessive growth of claws. Skin changes do not itch!! Excessive dandruff, muscle atrophy, cachexia

  • uveitis, epistaxis

Diagnosis:

• Direct confirmation finding amastigotes in smears from skin scrapers of ulcers, biopsy from lymph nodes, splenic aspirates, bone marrow.

• Serological: IFAT, ELISA, Western blotting, direct agglutination assays

• PCR

• Cytology - samples from LN, spleen, skin, bone marrow - Giemsa stain/quick stain. - can be confused with T. cruzi, can be uneffective due to low number of parasites, intradermal test.

Treatment:

• Most cases of CL heal without treatment - immune to further infection

• Other forms of L are extremely difficult to treat, long course and relapses.

• Medical treatment of infected dogs is ineffective in eliminating the parasite.

• Milteforan, Pentavalent antimony drugs and allopurinol (in norway).

Therapy in dogs have negative side effects, high cost, long term and often relapses. Today the the eradication of canine leishmaniosis is not reachable, but control measure can reduce the risk of infection.

Avoid sandfly bites through use of repellents and insecticides (spot on, collar, spray). Killing symptomatic + seropositive dogs. Vaccination control (canileish).

Visceral Leishmaniosis

L. donovani complex, L. infantum complex

• Most severe form of the disease, may be fatal if untreated

Signs: Fever, Anemia (Low RBC) weight loss, enlarged spleen and liver, dark discoloration of skin. Non-typical so can be difficult to see, can take a long time for signs to occur.

Even after successful treatment of this form, there can occur a form later called post-kala-azar cutaneous leishmaniasis.

Visceral - L. infantum, typical reservoir is dog, in some endemic areas up to 50% of dogs are infected.

In europe, middle east - in some areas with higher chance of canine leishmaniasis - L.infantum can be seen in cats + horse as cutaneous lesions.

Cutaneous Leishmaniasis

L. tropica, L. major, L. aethiopica

• Most common form - characterized by one or more sores, papules or nodules on the skin.

• Sores can change in size and appearance over time.

• Often described as looking somewhat like a volcano with a raised edge and central crater

• Sores are usually painless but can become painful if secondarily infected

• swollen lymph nodes may be present near sores (under arm ex.)

• Most sores develop within a few weeks of the sandfly bite, however they can appear up to months later

• skin sores of cutaneous L, can heal on their own but can take months or yars

• sores can leave significant scars, and can be disfiguring

• If infection is from L. tropica, it can spread to MM - upper lip to nose.

Process: sandfly bite → injects leptomonad form of parasite → multiplies inside skin cells (MF) → skin reacts (thickens + inflammation) → gets damaged and forms skin ulcer with hard edges, and can get secondarily infected. Over time, body starts healing (granulation). Heals, but leaves dark, sunken scar.

Mucocutaneous Leishmaniasis

L. mexicana, L. brasiliensis (rodents)

An infected sandfly bites and injects parasite (leptomonad) → leads often to skin sore (ulcer) forming → spreads to MM (nose, mouth, larynx etc.), parasites cause inflammation, necrosis, later reactive fibrosis.

Secondary effects can occur, like edema, deep erosion locally, spreading to lungs or other places, heals with fibrosis.

• leads to disfiguring lesions, general illness (fever, pain, anemia), severe cases spread to lungs → pneumonia or septicemia

Occurs with leishmania species from central/south america. This type occur if cutaneous lesion on face spreads to involve nose or mouth. This rare involvement may occur if a skin lesion near mouth/nose is not treated. Can occur months/years after original skin lesion. Hard to confirm dg. as few parasites are in the lesion.

4. Giardiasis and spironucleosis

Classification: Phylum: Metamonada, class: Trepomonadea, Order: Diplomonadida, Fam: hexamitidae, Genus: Giardia, spironucleus

Main Giardia Species:

• G. duodenalis – mammals; has 8 genotypes

  • G. enterica, G. canis, G. bovis, G. cati, G. simondi

• G. agilis – found in amphibians, birds, reptiles; long/narrow trophozoites, long median bodies

• G. muris – rodents, birds, reptiles; small paired median bodies, rounded

• G. ardeae – birds

Trophozoite Morphology

• Shape: bilaterally symmetrical, pear-like

• 2 nuclei, 4 pairs of flagella - motility like falling leaf, fibrils, pair of median bodies (darkly stained), adhesive disk (not always evident)

• No mitochondria or golgi-apparatus

• dorsal - convex, ventral - concave.

Cysts Morphology

• Shape: Oval

• Distinct cell wall set apart from cytoplasm

• 4 nuclei at anterior end

• fibrils, median bodies

• Each cyst → 2 trophozoites

Location: Small intestine

Final Hosts: Mammals, birds, reptiles (Zoonotic!)

Worldwide

Epizoo: Peaks around spring and autumn.

Transmission by contaminated food/water, fecal-oral via cyst ingestion.

Life Cycle - Direct cycle (single host), Infective stage is cyst, replicative stage is trophozoite in SI.

• Ingestion of cyst → excystation in small intestine → each cyst releases 2 trophozoites which multiply via binary fission on surface of intestinal villi → encyst in colon → cysts shed in feces.

• prepatent period: short (2 weeks in cow) - time it takes for infected to get cyst in feces.

Pathogenesis:

• Opportunistic, characterized by catarrhal gastroenteritis (esp. in young), intestinal disorder, diarrhea, nausea, abd. distension & weight loss.

• Trophozoites will attach to mucosal surface by disc → damage

  • Shortening of Villi (villus atrophy), crypt cells enlarge, inflammation, immune cells move into tissue.

  • Malabsorption, enzyme deficiencies (lactose intolerance), mechanisms of damage (mechanical irritation, blocks absorption)

Symptoms - range from asymptomatic to severe diarrhea/malabs.

• We can divide into acute (inc. 5-6d, lasting 1-3w. General signs like diarrhea, pain, vomit), & chronic (recurrent, malabsorption, weak/weight loss)

G. duodenalis: Infects cells of SI blocking nutrient abs. If clinically manifested, GI symptoms include diarrhea (watery, steatorrhea, pale, foul), often alternating with constipation, spastic pain in epigastric region, flatulence.

• soft diarrhea containing mucus, bad smell, greasy

• Not fatal for humans in developed countries, resolve on its own. (General GI signs)

Diagnosis

• Flotation method with zinc sulfate (Faust sol.), scan microscope 40x. for cysts (trophozoites can be present - acute)

• Minimum 3 fecal exams in 5–7 days (cysts - intermittent shedding)

• PCR for confirmation - Amplify TPI, GDH or BG genes

Treatment

• dogs/cats: Fenbendazole or Febantel (Panacur) for ≥3 days, metronidazol (metrobactin 500tbl).

• Follow-up fecal exams essential

Prevention: Cleaning measures, cysts are resistant and can survive for months in the environment, flies - mechanical, passive vector, Nutrition - protein suppresses giardiasis, carbs supports.

Prognosis: most recover well, dubious prognosis in immunosuppression (if immune system is weakened, then the result is more uncertain)

SPIRONUCLEUS (Hexamita/hexamitiasis)

Order: Diplomonidida, Family: Hexamitidae, Genus: Giardia, Spironucleus

Main Species & Hosts:

• Hexamita melagridis – turkey, quail, pheasant

• H. columbae – pigeons

• H. muris – mice, rats, voles, hornets

• H. salmonis and H. truttae – fish

So FH: Mainly birds (turkey, quail, pheasant, duck), Some species affect fish

Morphology:

• Trophozoites: Binucleated, 8 flagella (6 anterior, 2 posterior), No ventral adhesive disk

• Cysts: Oval, 8 nuclei, Immobile, contains 4 trophozoites

Location: Liberkühn crypts of small intestine, cecum, Bursa of Fabricius, liver, abdominal cavity

Epizo - Transmission: Ingestion of cysts (fecal-oral route)

Life Cycle: Binary fission of trophozoites in intestine → cysts passed in feces (similar to Giardia LC)

• reproduction by longitudinal division, forming oval 8 nuclei cysts

Pathogenesis & CS - non-specific:

• Diarrhea - watery - yellowish later, duodenitis, enteritis, weight loss, dehydration, death

• Ruffled feathers, high mortality in young animals (up to 80%)

• L. meleagridis - may die in coma or convulsions, bulbous dilatations of SI filled with water contents, rapid weight loss despite eating.

• Incubation period: ~1 week

Diagnosis:

• Detection of trophozoites/cysts in intestinal droplets (staining, e.g., haematoxylin)

• Post-mortem - autopsy: catarrhal inflammation in SI, fluid in intestine

Treatment & Prevention: No known treatment

Prevention: Hygiene, good nutrition, separate breeding of young birds (turkeys)

5. Histomonosis

Species: Histomonas meleagridis ("Blackhead Disease") - specifically causes histomonosis (Enterohepatitis infectiosa meleagridum)

Taxonomy: Phylum: Metamonoda, Class: Trichomonadea, Order: Trichomonadida, Family: Monocercomonadidae, Genus: Histomonas

Morphology:

• Similar to Trichomonas: nucleus, flagellum

• Three developmental stages:

  1. Luminal: in cecal lamina of birds, variable shape, one flagellum

  2. Transitional/Amoeboid: tissue-invasive stages (cecal wall, liver), spheroid, no flagella, with pseudopodia (“false feet” temp- foot like projections - for moving)

  3. Spheroid resting stage: in Heterakis eggs, small, non-flagellated

Location in Host: Cecum and liver

FH: Mainly turkeys, Occasionally chickens, guinea fowl

Vector / IH: Heterakis gallinarum (paratenic host)

Worldwide

Epizoo:

• No cyst formation

• Indirect transmission: via embryonated Heterakis eggs (viable >2 years in soil, also via earthworms)

• can also be by cloacal drinking - birds sit on freshly excreted feces of infected birds

Life Cycle:

• Indirect route (via Heterakis):

  • Histomonads are shed in feces of infected birds → the nematode (heterakis gallinarum) eats them → histomonas enters nd survives inside the eggs → passed in feces → survive in soil → turkeys ingest the eggs → invade ceca → travels to liver.

• Direct route:

  • Bird-to-bird contact, especially through cloacal drinking

Pathogenesis & Clinical Signs:

• High morbidity and mortality, especially in 14 weeks old turkeys (up to 100%). Birds that recover get irreversible changes to cecum/liver (scarred).

• Incubation: 2–3 weeks

• Signs in turkeys: apathy, ruffled feathers, sulfur-yellow feces, cyanosis (head, comb, wattles) → “black head”, circulatory issues

  • Dies within 1-2 weeks untreated

• Chickens: more resistant, often asymptomatic or mildly affected, can develop severe liver damage, can also be infection of ceaca with Eimeria tenella.

Diagnosis:

• Post-mortem: lesions in mucosa (as histomonas get into caecal wall), thickened → necrotic, exudate made that become solid, hard cheesy plugs. Findings are confirmed by histology.

• PCR, Culture detection.

• Differential diagnoses must be considered (candida albicans ex.)

Treatment & Control:

• No approved antihistomonal drugs in Europe

• Paromomycin and alternative antibiotics may be used in feed at conc. 400ppm (permitted EU reg. 37/2010)

measures:

• Keep turkeys separate from chickens

• Maintain hygiene: disinfect floors, feeders, drinkers

• Keep litter dry, use wire/slatted flooring, Disinfect and renew litter before restocking

• systematic control of h. gallinarum infection, coccidiosis - eimeria.

• prevent by not keeping turkey on ground used before by chickens (need to be several years apart), rotate ranges, cecal worm control

6. Bovine and Avian trichomonosis

Taxonomy: Phylum: Parabasala, Class: Trichomonadea, Order: Trichomonadida, Family: Trichomonadidae, Genera: Tritrichomonas, Trichomonas, Pentatrichomonas

Main Species:Tritrichomonas foetus (strain B – bovine), T. foetus (strain C – feline/cats) & T. gallinae, but we also have T. vaginalis & tenax, Pt homonis.

Morphology - parabasala

• Named after parabasal apparatus (developed Golgi body connected to nucleus by fibrils)

• generally a return flagella - forms undulating membrane - supported by fibrils (costa)

• No cystostoma, phagocytosis - whole surface of cell.

• Hydrogenosomes (energy metabolism) instead of mitochondria

• Pear-shaped body with:

  • Axostyle running through the cell axis

• Flagella: Greatest variability among species

  • Bovine: 3 anterior + 1 posterior

  • Avian: 4 anterior

• They DO NOT create true cysts

• Some (T. foetus, T. muris) can form pseudocysts

• Infective stage: trophozoite

The order Trichomonadida:

• Parasites of genital & digestive tract of vertebrates

• contain one nucleus, oval shape, axostyle, parabasal body, 4-6 flagella

• Asexual reproduction, longitudinal fission

• Anaerobic

Ditricomonas (dt) - 2, tritrichomonas (Tt) - 3. tetratrichomonas (T) - 4, pentatrichomonas (Pt) - 5.

Causative agent: tritrichomonas foetus B (bovine strain)

Bovine Trichomonosis:

Location: Reproductive tract

FH: Cattle

Transmission: Sexually transmitted via coitus, artificial insemination, and gynecological exams. Bulls act as source of infection!

Life Cycle

• Direct life cycle, no environmentally resistant stages

• Mobile trophozoites multiply by binary fission

• coitus → trophozites colonize vaginal mucosa → cervix → infect bulls during mating → in preputial mucosa of bulls → form pseudocysts

Pathology: Vestibulovaginitis catarrhalis purulenta, endometritis catarhalis purulenta, idiopathic abortus, pyometra, disorders of reprod. & sterility.

Clinical signs:

• Cows: Early abortion (2-4 months), uterine discharge, irreg. estrus cycles, purulent endometritis, pyometra, sterility

• Bulls: Preputial sac inflammation, small nodules, chronic - no gross lesions.

  • Bulls >3–4 years: lifelong carriers, may recover spontaneously (asymptomatic)

  • Bulls <3–4 years: transient infection

Diagnosis: direct confirmation

• Based on clinical history and lab tests

• Number of parasites varies, highest at 14-18 days post infection (in vaginal mucosa).

• Parasites are present 2-3d before estrus and 1 week after (in vagina)

• Abortus in 8-16th week of gravidity (in aborted fetus)

• Samples: Genital fluid, placental fluid, aborted fetus, uterine washing, pyometra discharge (in case of abortion), while in infected herds, do preputial/vaginal washings/scrapings.

• Microscopy: jerky, rolling motion

• Methods: Native prep, Stained smear, Culture, PCR

Treatment

• WOAH-listed (need to report)

• Symptomatic treatment only

• Nitroimidazoles (not registered for use) (metronidazol, dimetridazol)

• resistant to penicillin, streptomycin + many other ATBs.

Prevention & Control

• Use trichomonad-free bulls for artificial insemination

• Strict biosecurity measures

• Regular cleaning of urine and manure (parasite can survive for days)

• Control bull health and disinfect AI instruments

• TrichGuard vaccine available

Avian Trichomonosis:

Causative Agents: Trichomonas gallinae

• Tetratrichomonas gallinarum

• Tetratrichomonas anatis

• Tetratrichomonas ansertis

Morphology:

Location in Host: Cranial GIT: mouth, crop, pharynx, esophagus, proventriculus

FH: Mainly pigeons worldwide (up to 80% of older birds are asymptomatic), turkeys are frequently infected, domestic chickens are rarely. But also found in other birds, like parrots.

Epizoo:

• Pigeons: transmission due to regurgitated crop feeding - “crop milk” to offspring.

• hawks: ingestion of infected birds

• Other birds: By contaminated drinking water

Life Cycle

• Direct life cycle

• No environmentally resistant stages

Pathogenesis & Clinical signs

• Characterized by: Mucopurulent inflammation + Formation of pseudomembranes and nodules in:

  • Beak, sinuses, pharynx, esophagus, throat

  • generally lesions in beak cavity, sinus, pharynx, esophagus, crop and stomach

• Yellow necrotic lesions in upper GIT

  • Yellow buttons - liver & heart (caseous necrotic foci) in pigeons

• fatal in pigeons (2-4 weeks old)

Acute Phase

• Necrotic masses - first lesions appear in mouth, pharynx, esophagus, crop, consisting of Creamy-white, sticky exudate

• Lesions progress to small, raised yellow-white ulcers

Chronic Phase

• Lesions enlarge, become hard and caseous

• May invade sinuses, extend externally to beak, eyes

• Can penetrate base of skull → affect brain and viscera

• can lead to Necrosis in liver, spleen, pancreas, heart, lungs, air sacs

Diagnosis

• Crop swab → direct smear → microscopy of wet/stained smears, culture

• In dead birds: Take smears from the layer bw. normal and affected tissue or from exudate of body cavity

Treatment

• Nitroimidazole compounds: Metronidazole, Dimetridazole, Ronidazole

  • Only authorized for non-food birds (e.g., carrier pigeons)

Prevention & Control

• Sanitation of water and feeding systems

• Prevent contact between pigeons and other wild/domestic birds

• Eliminate contaminated water sources

• Regular monitoring and isolation of infected birds

7. Pathogenic and potential pathogenic Amoebae of animals and humans

Phylum: Amoebozoa, Class: Entamoebidae Lobosea, Order: Entamoebida, Family: Entamoebidae, Genera: Entamoeba, Endolimax

The order Entamoebida include:

• E. histolytica (colon, liver) - humans, dogs, cat, pigs, rats

• E. polecki - pig, goat and humans

• Dientamoeba fragilis (cecum and colon)

• Naegleria spp. - nasal cavity, olfactory nerves, meninges

• Acanthamoeba spp. - skin, resp., urogenital, meninges

• Balamuthia spp. - subacute, chronic form (acanthomoeba like)

Amoebae varies highly in shape (plasma membrane), nucleus with chromatin granules on nuclear membrane, moves by pseudopodia, feed by phagocytosis, are heterogenous, either parasitic or free living. Many form cysts.

1. Entamoeba histolytica (Pathogenic - causes Amoebiasis)

Morphology:

• Trophozoite: Ingested RBCs, Nucleus with central karyosome and divided peripheral chromatin. Pseudopod.

  • 2 types: forma minuta (non-pathogenic) & Forma magna (pathogenic)

• cysts: 1–4 nuclei (infective → quadrinucleate cyst)

Location: Cecum and sigmoidal rectal region of man.

• Primary: colon - dysentery, ulceration (forma minuta)

• Extraintestinal: Hepatitis, abscess, icterus (forma magna)

FH: Dogs, cats, pigs, humans (zoonotic)

Geography: Cosmopolitan
Transmission: Fecal-oral - hand-to-mouth
Life Cycle (direct):

• Cysts ingested → excyst in small intestine → trophozoites in colon → binary fission → new cysts in feces.

• Can invade intestinal wall → bloodstream → liver, brain, lungs.

Pathogenesis & Clinical Signs

• Mostly asymptomatic, ranging to intestinal.

• can develop to progressive invasive disease (young adults)

• intestinal disease - small ulcers - colitis, perforation of intestine

  • acute fatal amoebic dysentery, Hepatic abscess

• appendicitis, toxic megacolon, amebomas (thickening of intestine wall around abscess)

  • Extraintestinal form: liver abscess (chocolate-colored, pus, necrotic, bacteria free), peritonitis, skin and genital lesions, pulmonary abscess

  • Ameba-free stools common, metastasis via blood, primarily liver affected.

Diagnosis

• Fecal exam (trophozoites/cysts), serology (IHA, ELISA).

• liver enzyme profile is usually normal. blood tests (RBC phagocytosis)

• Abscess aspiration (anchovy paste, aspirate for tropho)., culture, radiologic (CT)

Treatment

• Nitroimidazoles (ex. metronidazole), chloroxin, paromomycin.

• Prevention: Hygiene, avoid contaminated food/water.

• endemic area: boil/cook water, treat water, clean uncooked fruit/veggies

2. Naegleria fowleri (“Brain-eating amoeba”, free-living)

Mainly affects young, normal immune system, healthy individuals. FH: humans. Worldwide.

Morphology: Trophozoite (infective), flagellate (CSF), and cyst forms.

Location: Nasal cavity → olfactory nerves → brain

Transmission: Free-living, found in water/soil

Life Cycle: Trophozoite enters via nasal cavity → travels to brain → phagocytizes RBCs/WBCs. Replicates by Promitosis.

Clinical Signs: inc: 3-7d. PAM (Primary Amoebic Meningoencephalitis)

• sore throat, intense headache, fever, nasal blockage, vomiting → coma in 3–4 days. Fatal.

Diagnosis: Biopsy, CT scan
Treatment: Mostly fatal, limited success with treatments.

3. Acanthamoeba spp.

Affects immunodeficient, weakened individuals. FH: humans. Worldwide (freshwater, brackish, sea).

Morphology: Trophozoite and cyst forms. Vesicular nucleus, large endosome. cytoplasm.

Transmission: Enters via broken skin, respiratory, urogenital tract. Spreads by blood to brain and meninges. Found in pools, hot tubs, tap water.

Life Cycle: Trophozoites replicate via mitosis (nuclear membrane breaks down). Both stages may infect by skin, eyes etc.

Clinical Signs: GAE (Granulomatous Amoebic MeningoEncephalitis)

• Cutaneous papules, nodules, ulcers, sinusitis, cephalalgia, meningeal signs, OFTEN infect ocular cornea, keratitis, uveitis, blindness.

Diagnosis: Eye scraping (keratitis). CT, biopsy for GAE.

Treatment: GAE is usually fatal.

8. Eimeriosis of cattle, sheep, and goats.

Taxonomy: Phylum: Alveolata, Subphylum: Apicomplexa, Class: Coccidea, Order: Eimeriida, Family: Eimeriidae, Genus: Eimeria

Apicomplexa: Obligatory intracellular parasites, single-celled, parasitic, medically important, strict specificity of host, topic/organ and age, simple nucleus, no cilia/flagella. Supphylum is characterized by presence of apical complex found at apical end of the sporozoites and merozoites.

• Zoit (sporo/mero): gliding moving, actively searches the target cell

• Oocysts: immobile, internal structure depends on spp.

• Apical complex: polar rings, conoid (fibrillar structure under), subpellicular microtubules (from the ring, serve as support for locomotive fc.), rhoptries, micronems + dense granules (release enzymes that help go into host) - rhoptries + micronems + the granules → secretory glands → help enter host cells.

LC: Monoxenous (one-host LC). Same in Eimeria, Cryptosporidium, isospora.

1. Merogony/schizogony (produces merozoites)

   • Host eats sporulated oocyst → sporozoites are released into gut cells → trophozoite which develop into meronts → inside meront, nuclei asexually reproduce → releasing merozoites from ruptured gut cells, then invade other cells.

   • B. Bovis 1st: endothelial cells of posterior half of SI. 2nd gen: meronts in cecal and colonic epithelium. Gamonts in epithelial cells of cecal and colonic gl.

   • B. zuernii 1st: through SI. 2nd: LI. Gamonts colon and cecum.

2. Gametogony (produces gametocytes)

   • Sexual reproduction. Merozoites → gamonts through gametogony. Female macrogamete + male microgamete → karyogomy → diploid zygote → forms oocyst wall → unsporulated oocyst released through feces.

3. Sporogony (produce sporozoites)

   • Environmental, unsporulated oocysts are excreted into feces → sporulation occur outside host → form sporocysts with sporozoites inside.

Bovine Eimeriosis (Cattle), worldwide

Main species (all are pathogenic)

• E. bovis -posterior SI. Very pathogenic

• E. zuernii - SI

• E. auburnensis - SI

Morphology:

• Trophozoites: No flagella/cilia, simple nucleus

• Cysts: 4 sporocysts with 2 sporozoits each. Small, oval shape, 2 thin shells, unsporulated (if fresh) or sporulated, transparent in color.

• Oocyst - microphyle at one pole where sporocysts are released

Location: Intracellular, in intestines.
Epizoo/Transmission: Ingestion of oocyst, fecal-oral route.

• Coccidiosis is commonly a disease of young cattle (1-2 months to 1 year) and is usually sporadic during the wet season of the year. Cattle confined to feedlots are susceptible to coccidiosis throughout the year. All Eimeria are pathogenic.

Clinical signs:

E. bovis: Death within 3-4 weeks.

• Diarrhea, tenesmus, fever, congested mucosa, often edematous and hemorrhage.

• partial immunity following recovery

E. zuernii:

• Bloody diarrhea

• Death beginning 7d of onset of symptoms, may not be passing oocyst at this time.

Diagnosis: Flotation method.

Treatment: Amprolium corid, Sulfaquinoxaline, sulfamethazine for 5 days.

• Prophylaxis of coccidiosis in cattle: Lasalocid bovatec, decoquinate deccox, monensin rumensin.

Eimeriosis of sheep and goat, worldwide.

Sheep: E. Faurei (SI), E. intricata (SI/cecum), E. ovina (SI), E. ovinoidalis (colon)

Goat: E. arloingi (crypts), E. ninakohlyakimovae (crypts), E. christenseni (SI)

Location: SI

Epidemiology: Coccidia are common and normally present in animals of all ages. Most adults don`t get sick becuase they quickly develop immunity.

• Lamb coccidiosis: occur in young lambs as they are very susceptible. Outbreaks occur in age of 4-8w.

• Eimeria spp. are host specific and not transmitted from sheep to goat.

Clinical signs:

• Outbreaks - lambing pens, crowded feedlots, after stress

• Signs by dirty tail (mild diarrhea), loss of appetite, weak & poor growth, bloody diarrhea in severe case

• some goats can be constipated, and die suddenly without diarrhea

• Eimeria destroys the intestinal epithelium, reduces absorption of nutrients → diarrhea, dehydration, severe hemorrhage.

Diagnosis: Fecal flotation and PM intestinal scrapings.

• oocysts are common in healthy animals, thus we cannot diagnose based on presence alone. Healthy lambs have 100 000/g and look fine, while if in the case of coccidiosis, we may have diarrhea and over 20 000 pathogenic oocysts/g.

Treatment and prevention: sulfonamide for treatment, monensin as prevention. Clean pens and good hygiene, do not mix different age groups. 

9.Eimeriosis of rabbits and hares.

Eimeriosis in rabbits (FH: rabbit)

Main species:

• E. intestinalis – Intestinal. Highly pathogenic!

• E. flavescens – Highly pathogenic! Cecum

• E. magna

• E. media

• E. piriformis – LI

• E. stiedai – Liver

Location: intestine and liver

Life cycle:

Epizoo: Occur commonly during time of weaning and in high populations like rabbit farms.

Clinical signs:

• characterized by enteritis, hepatitis, high young rabbit mortality.

• depression of animals → anemia, releasing of fluids, watery feces, dehydration, weight loss (convulsions/paralysis in severe case), LI more commonly affected, can be congested, hemorrhagic or edematous.

• Typ. infections with intestinal coccidiosis are mild, often no CS seen.

E. stiedai: Invade intestinal mucosa → enter BV → transported to liver → bile ducts. Cause hepatic infection, incterus, edematous enlargement and blockage of bile duct. Small white nodules can be found on the liver parenchyma. Hepatomegaly may be seen.

Diagnosis: Oocyst in feces - flotation method, PCR to identify, or by post mortem.

Treatment: Diclazuril, Monensin, Toltrazuril, Sulphonamids. Good hygiene.

Hare

Main species: E. townsendi & E. leporis

• Clinical manifestation in wild hares are rare, but may occur in wet season in young hares (as wet wather → oocyst survive well, more infective spores are present, higher chance of disease/exposure).

10.Describe Eimeriosis in poultry.

Main species, Location: Intestine, Worldwide, first 3 are most common.

• E. tenella - chicken/cecum, highly pathogenic, cause bleeding → anemia. Most common in fattening chicks. Dead in 4-6d p.i.

• E. acervulina - SI, duodenum, formation of lesions - white spots.

• E. maxima - chicken/jejunum, ileum

• E. necatrix - chicken/jejunum, ileum, caeca

• E. praecox - chicken/SI

• E. brunetti - chicken

• E. danilovi - duck/SI

• Turkey: E. adenoides (LI) E. meleagrimitis (SI), E. gallopavonis (multiplies in cecal pouches), E. truncata (kidney)

Chicken Eimeriosis:

Epizoo: Primarily in chicks in high conc. on small areas, mostly in young. Cause economic loss in the industry due to decr. weight gain. Highly resistant oocyst form in the litter. Oocyst vary in size, E.maxima is largest, E. mitis is smallest.

Life cycle: Same as in cattle. 3 generations of merozoites.

• E. tenella: schizonts I. gen. - 900merozoites, 2nd. gen - 300 merozoites, 3rd gen. gamogony.

Patho/CS:

• Characterized as catarrhal-hemorrhagic enteric disease

• Diarrhea, CNS disorders, Anemia

• Decr. growth, formation of nodules

• Pathology due to the destruction of intestinal cells, each sp. has tissue site specificity

• E. tenella - quick, bleeding into lumen of cecum, whitish mucosa, cecal cores of clotted blood.

Diagnosis:

• Intra vitam: coprological examination - flotation method - find oocysts

• PM: Look for scratches of the epithelial layers of the intestine, histological sections, we can see villus atrophy, crypt hyperplasia and incr. WBC infiltration.

Treatment: Anticoccidal agents such as amprolium, sulphonamides, clopidol, inophores or toltrazuril.

• ATBs - tylosin, amoxicillin

• supportive care

• environmental/management changes, slow down sporulation by removing feces and soiled bedding, keep them dry. Vaccine (livacox) - gel vaccine

11.Eimeriosis and Cystoisosporosis of pigs

Eimeriosis in pigs: (Small intestine, found worldwide).

Main species: E. scabra, E. suis

• E. debliecki, E. neodebliecki, E. spinosa, E. poliata

Life cycle:

Patho/CS:

• Acute enteritis limited to lower SI, loss of condition, perianal staining.

• characteristic yellow fibronecrotic pseudomembrane often accompanied by bloody diarrhea.

Diagnosis: Diagnose during acute prepatent phase (8-10d) by examination of gut. Fecal floation.

Treatment: Anticoccidials.

Pig cystoisosporosis/isosporosis – Cystoisospora suis

Order: Eimeridia, Fam: sarcocystidae, Genus: cystoisospora, sarcocystis

• Location: SI, FH: Pigs, piglets, Worldwide, common in North-america, Europe & Australia.

• note: isospora is same order but monoxenous

Morphology: Oocyst with 2 sporocysts with 4 sporozoites each (8 in total). Small, oval, 2 thin shell, unsporulated, transparent. No stieda body.

Epizoo/transmission: Fecal-oral route.

• Short development cycle of C. suis and high susceptibility in young animals! Most common coccidosis of pigs. Prepatent period is 4-7 days

Life cycle: Occur in mucosa of small intestine. Heteroxenous - need more than one host to fully develop! Can also be monoxenous.

• Sporogony: sporulates in the environment (20-40degrees) → sporulated oocyst are very resistant to most disinfectants, can have paratenic host (rodent).

• Merogony: sporulated oocyst is eaten → release of sporozoites into villous epithelium → merogony process, merozoites produced in 3 generations.

• Gamogony: gametocytes → oocyst is released to the lumen of intestine and shed with feces.

Patho/CS: 1. villous atrophy and fusion, 2. necrotic enteritis, 3. enterocyte metaplasia, 4. crypt hyperplasia.

• Presence of C. suis in different developmental stages in the cells of the intestinal epithelium.

• Lesions encourage the invasion of secondary pathogens since the protective function of the mucosa is damaged.

• The intestinal mucous regenerates quickly, but the digestive function will be damaged for longer than the clinical disease due to the fact that it will take time for the villi to grow back to their original size.

• clinical: Piglets will have pasty to watery diarrhea, yellowish to gray in color, blood is never present, gains less weight, often having secondary infections. Adults are asymptomatic.

  • short development cycle of C. suis, high susceptibility of young

Diagnosis: direct examination of fecal smear, accumulation and flotation of oocysts, autofluorescence microscopy, quantitation in McMaster counting chamber, necropsy - scraping of gut mucosa & histology.

Treatment:

• Coccidiosis in piglets are unresponsive to antibiotics.

• Toltrazuril 5% suspension (against neonatal coccidosis), Ponazuril, Diclazuril, Sulphidamidine. Hygiene measures are important in control of piglet coccidiosis. Single oral treatment with Baycox in the first week after birth is necessary. 

• diff. dx: need to consider other enteropathogens like E.coli, coronavirus, rotavirus etc.

12.Cystoisosporosis of carnivores.

Coccidian parasites that infect the intestine of dogs and cats.

Phylum: Alveolata, Subphylum: Apicomplexa, Class: Coccidea, Order: Eimeridae, Family: Sarcocystidae, Genus: Cystoisospora

Main species (Epithelium of SI, Worldwide)

• Dog: C. canis (36um), C. ohioensis (24um), C. burrowsi, C. neorivolta

• Cat: C. felis & C. rivolta (larger oocyst than felis)

Morphology: Oocyst is small and oval, has 2 sporocysts, each containing 4 sporozoites (Total = 8). 2 thin shells, transparent when unsporulated.

• No stieda body, very host specific.

• Sporulation depends on O2, humidity + temperature. After sporulation, oocysts → very resistant to disinfectants.

FH: Dog, Cat. (Not found in eq, ru or poultry)

• Rodents as paratenic host.

Transmission: fecal oral route, ingestion of cyst.

Life cycle: can be monoxenous (one host) or heteroxenous (with Paratenic host)

• Sporogony (exogenous): Unsporulated oocysts shed in feces → sporulation in environment → sporulated oocyst is eaten by FH, excyst in SI, releases 4 sporozoites that invade the epithelial cells.

• Merogony: in epithelial cells → merozoites, reproduce by binary fission. Epithelial cells rupture and releases merozoites → infects new cells.

• Gamogony: Merozoites become macro and microgametes which fuse to form a zygote → unsporulated oocyst shed in feces

• Paratenic host: rodents can ingest oocysts → inside, the parasite forms a dormant cyst (hypnozoite), no disease occur. But FH can be infected by eating the rodent.

Patho/CS:

• Mild infection: often no symptoms

• Severe infection (esp. C. canis): in puppies 3-4 weeks - 4m. old.

  • GIT issues: Bloody diarrhea, vomit, anorexia, apathy, abd. pain - hemorrhagic enteritis

  • fever, dehydration, polyuria, anemia, poor growth.

  • can look similar to parvovirus.

• Inc. period: 1week

• immunity in cats: 2-5months (temporary)

Diagnosis: Coproscopy (fecal exam) detection of unsporulated oocyst. Flotation method with FAUST.

Treatment: Sulfadimethoxine, toltrazuril, ponazuril. Hygiene, remove feces, disinfection of breeding areas, not feeding of raw meat.

13.Cryptosporidiosis of mammals and birds.

Classification: Phylum: Alveolata, subphyl: Apicomplexa, Class: Coccidea, Order: Cryptosporida, Fam: cryptosporiididae, genus: cryptosporidium

Species:

• C. hominis – humans

• C. parvum – ruminants, humans, rodents

• C. bovis – cattle, sheep

• C. andersoni – ruminants (abomasum)

• C. suis – pigs

• C. canis – canids

• C. felis – cats

• C. muris – mice, birds

Birds (3 species)

• C. baileyi – chickens (respiratory tract, intestine - cloaca, rectum, kidney, conjunctiva, bursa of Fabricius)

• C. galli – chickens (stomach)

• C. meleagridis – turkeys (intestine, occasionally other organs)

Within the genus, we distinguish 2 morphologically different groups:

1. Small oocyst group (infects intestinal enterocytes): C. parvum, hominis, canis, felis, bovis, suis

2. Large oocyst group (infects stomach glands): C. muris, galli

Morhology:

• Extremely small (5–7 µm), smaller than Eimeria

• Oocysts are: round, light pink, 2 thin shells, sporulated (4 free sporozoites). No sporocysts.

• microgametes - lack flagella

• Low host specificity - many spp. are zoonotic.

Location in Host: Microvillous of the digestive tract (intestine, gastric wall), respiratory tract.

• Intracellular extracytoplasmic localization: development - parasite (sporozoite) attaches to cell → host cell membrane wraps around → vacuole forms → parasite is inside host cell but not in the cytoplasm, sitting in a pocket.

Hosts: Mammals & Birds (Worldwide)

Epizoo: C. parvum & C. hominis = Zoonotic, cryptosporidium infections in both immunocompetent + immunocomprised individuals. C.parvum also affect healthy people.

• Global prevalence ≈ 10%, zoonosis, human & animal genotypes

• oocysts are often found in rivers, lakes, ponds etc. difficult to remove and hard to kill, drinking water - amplifier. Up to 20% of general population can be considered at higher rislk.

Transmission: Fecal-oral route, Foodborne & waterborne diseases - contaminated water + food carries it.

Life Cycle: endogenous → asexual + sexual reproduction and sporogony occur inside the host. Monoxenous.

Pathogenesis

• Hypertrophy of crypt cells

• Abbrevation of villuses (shortening)

• Inflammation in Lamina propria mucosa

• increased water secretion by crypt cells → diarrhea, no enterotoxin involvement.

Clinical Signs (calves): Profuse watery (mucus, fibrin..) diarrhea, complete destruction of microvilli of intestine, light-yellow feces, salivation, anorexia, acidosis, fever, apathy, weakness, frequent defecation, foul-smell. inc. 5-8d.

Clinical Signs in Humans: Serious in young, pregnant, patients undergoing chemo + elderly. Can be fatal in immunodeficient hosts. Low infectious dose (LD₅₀ ≈ 130 oocysts).

• Watery diarrhea, stomach cramps, slight fever, weight loss.

Diagnosis: Look for oocysts under microscope, by floation method, stained microscope slides.

• other tests: Fluorscent Ab test (Ab with dye attach to parasite), ELISA.

• Stains used: Kinyoun`s Acid fast stain - pink/red oocyst on blue background, modified Ziehl-Neelsen stain (hot acid-fast stain) - red oocyst/sporozoites on green background.

Therapy in animals: Halofuginone (Halocur) for calves, nitayoaxanid (human), azitromycin, pyrvinium pamoate (dog/cat)

Supportive: IV fluids, Electrolytes, Proper nutrition

Duration: Inc. period: 1-12d. In healthy people, duration of symptoms lasts around 2w or less. There is no drug to cure cryptosporidiosis. Drink plenty of fluids.

Prevention: hand washing, proper sanitation, people should not drink contaminated water (swimming pool/lake)

• During outbreak: boil drinking water, eat only cooked foods, avoid unpasteurized milk and juices

14.Neosporosis

Classification: Phylum: Alveolata, Subphyl: Apicomplexa, Class: Coccidea, order: Eimeridae, Fam: sarcocystidae, genus: Neospora.

Species: Neospora caninum - cause bovine neosporosis

• very similar to Toxoplasma gondii in morphology + LC, but they infect different main hosts. Neospora has dogs (FH), cattle mainly affected. Toxoplasma has cats (FH). also, sexual reprod. occur in dog (FH) in neospora, while cattle, sheep + eq = IH.

Morphology: oocyst are round/slightly oval, with 2 sporocysts with 4 sporozoites each. Tachyzoites are in vacuoles of cytoplasm of cells. Tissue cysts - thick wall and oval.

Location: Multiply in the intestine enterocytes. Forms cysts in muscle tissue and neural tissue.

FH: dog, coyotes, wolves

IM: ruminants, horses. Mainly cattle.

Geography: First found in Norway in dogs, but exists worldwide. In cattle, occurrence is in cosmopolitan.
Epizootology: Fecal-oral route and Transplacental transmission in dog and cattle (most imp. in cattle - bovine neosporosis). Infection is usually life-long.

Life cycle: Indirect. Merogony + Gametogony in FH, Sporogony in environment.

Pathogenesis and clinical signs:

• Adult cow: Abortion (may abort from 3months of gestation to term). N.caninum induced abortions occur year round. Fetuses may die in utero, be absorbed, mummified, autolyzed, stillborn, or born clinically normal but chronically infected. Within herds, abortion may be clustered, sporadic or epidemic. Cows with N. caninum Ab (seropositive) are more likely to abort than seroneg. cows.

• Calves: Clinical signs only visible in calves younger than 2 months. Limbs flexed or hyper-extended, ataxia, decreased patellar reflexes, loss of conscious proproreception. Exophtalmia or asymmetrical appearance of eyes. Calves can be born underweight, not being able to stand, NS signs.

• Dogs: Muscular atrophy, ataxia, paresis, ascending paralysis, muscular pain in lumbal, pelvic region, torticollis, dysphagia, rigid muscle contraction. Infection in other organs → skin ulceration.

  • prenatal infection (infection may pass from mother to puppy during pregnancy → puppies born already infected → focal necrosis in brain, spinal cord + nerves → damage of NS)

Diagnosis: Serology → detects specific Ab to identify between neospora and T. gondii. Flotation method - coprology.

• CS (a lot of abortions in the herd lately), immunohistochemistry, PCR, Histopathology, examination of fetus for definitive diagnosis, differential diagnosis.

Treatment:

• Dogs: sulphonamides, clindamycin, toltrazuril.

• No drug effective against tissue cysts - for cattle and no effective treatment for preventing transplacental transmission in cattle.

Control: preventing animal contamination of feed, prevent contact with placenta/abortion tissues.

15. Sarcocystosis of mammals

Classification: phylum: Alveolata, Subphyl: Apicomplexa, class: Coccidea, Order: Eimeridae, fam: Sarcocystidae, genus: Sarcocystis

Predator-Prey LC.

Main species:

• S. bovihominis – cattle → humans

• S. cruzi (bovicanis) – cattle (IH) → dogs, wolf, coyote, etc. (FH)

• S. hirsuta (bovifelis) – cattle → cats

• S. suihominis – pigs → humans

• S. miescheriana (suicanis) – pigs → dogs

• S. tenella (ovicanis) – sheep → dogs

• S. gigantica (ovifelis) – sheep → cats

• S. suifelis, S. arieticanis, capracanis, hircicanis, equicanis, S. bertrami + neurona.

Characteristics: Named after IM host - then FH host. When FH is dog or cat, then it is not Zoonotic!

Morphology: Some can form macrocysts which is visible with naked eye. Oocysts contain 2 sporocysts with 4 sporozoites.

Location: Intracellular, develop cysts in striated muscles of IM host.

FH: dog, wolf, coyote, raccoon, fox and hyenas, and humans (in some)

IM: ruminants, pigs, horses

Geographical distribution:  Worldwide.
Epizootology: Zoonotic: S. suihominis, S. bovihominis. Sarcocystis with dogs or cats as FH are not zoonotic. Species transmitted by dogs are generally more pathogenic to IM host than those by cats. Fecal-oral route, ingestion of cysts.

Life cycle: Heteroxenous life cycle.

• Asexual stages in prey species, usual site of pathology.

• Sexual stages in predator - gemetogony in intestinal tract in FH, sporogony occurs within this host and infectious sporocysts with 2 sporozoites (4 each) are shed in feces.

• 2 host development = Endogenous (within host).

• shizonts/meronts in endothelium, tissue cysts in striated muscle of IH (cattle). 1 months P.I, mature at 2-3 months.

Pathogenesis and clinical signs:

• No pathology in definitive host (dogs, cats)

• Can be asymptomatic, diarrhea (rarely)

• the species that are transmitted by dogs are generally more pathogenic to IH than those transmitted by cats

• IH with acute and subacute sarcocystosis (rare, occurs only when the animal ingest a large number of sporocyst)

  • Symptoms: fever, apathy, anorexia, anemia, weight loss, decr. milk production, gen. lymphadenopathy, abortion.

• IH with chronic sarcocystosis: host usually shows no obvious CS/symptoms of disease

  • Micro: myositis (infl. of muscle tissue), degenerating cysts enclosed by granulomas + mononuclear infiltrations (immune system enclosing the parasite)

• Pathology: IH are the most affected, 20-40d after eating sporocyst → migrates throughout bv → acute lesions (edema, hemorrhage + necrosis) develop. Lesions are linked with the maturation of 2nd gen of meronts within endo + subendothelial cells.

Diagnosis:

• FH: coproscopic detection of oocyst/sporocysts in feces (flotation with faust), Morphological identification of species is not possible.

• serological: specific Ab in FH, IH.

• IH: PM (cyst in muscle) - digestive method - microcysts, macrocysts - meat inspection.

Treatment: No therapy for IH.

FH: Toltrazuril, diclazuril. Do not allow dogs to feed on raw meat, most common where home slaughter occurs. Prevent contamination of feed with dog feces containing sporocysts.

16. Equine protozoal myeloencephalitis (S. neurona)

EPM – equine protozoan myeloencephalitis – Sarcocystis neurona (infection of CNS)

Location: cysts in striated muscles. Brain and spinal cord of aberrant horse.

FH: Possum

IM: Small mammals. Horse is aberrant host.

• aberrant host = parasite can infect + develop abnormally but cannot complete its normal LC.

Geographical distribution: Worldwide, common in USA.
Epizootology: Horses get infected when ingesting possum feces.

Life cycle:

Pathogenesis and clinical signs: 

• CS: Incoordination, gait abnormalities, Head tilt, facial nerve paralysis, difficulty swallowing, loss of sensation along the face, neck and body

  • Weakness, lameness, weight loss, blind, seizure, asymmetric ataxia, focal muscle atrophy, urinary incontinence, acute recumbency, various nerve deficits

• Meronts → neural cells of brain + spinal cord → focal bleeding, necrosis + myeloencephalitis (inflammation)

Diagnosis: Clinical presentation + necropsy, serology, western blot-cerebrospinal fluid (CSF) is needed, PCR

• high seroprevalence (close to 50%) - more of healthy horses may test positive for exposure without ever developing clinical EPM. (due to latency/subclinical infection, so horse may not show signs)

Treatment: During 4-12 weeks administrated trimethoprim/sulfadiazine and pyrimethamine in feed. The therapy can result in side effects such as leukopenia, therefore, it should be given with vitamin B complex. More recently, we can also give diclazuril, toltrazuril and ponazuril. Anti-inflammatory drugs and vitamin E. Decrease exposure to possum feces.

17. Toxoplasmosis of animals and humans

Classification: phylum: Alveolata, subphyl: apicomplexa, class: coccidea, order: eimeridae, fam: sarcocystidea, genus: Toxoplasma

Main species: T. gondii (only species of the genus)

• Clonal population structures - different genotypes → 3 clonal strains (I, II, III)

• In LC → several infection stages

Morphology: 3 forms - sporozoite → tachyzoite → bradyzoite

• tachyzoite: pseydocyst IH. Rapid growing (endopolygeny). Seen in early stages of infection. Located free intracellularly. Most common in brain, skeletal & cardiac muscle.

• Bradyzoite: tissue cyst IH - due to host immune resp. Slow growing (dormant - ed). Infective. In brain, skeletal + cardiac muscle. Marks beginning of chronic phase. Resistant to low pH + dig. enzymes. Cyst wall → dissolved → bradyzoites infect tissue → tachyzoite.

Location: Intracellular. Infect nucleated cells, not erythrocytes.  

Host: Infects most species of warm-blooded animals, incl. humans → toxoplasmosis. FH = felines, IM = Bird, mammals. Humans = aberrant host (Zoonotic!)

Geo: Worldwide
Epizootology: Wide range of intermediate hosts, very narrow range of final host. Infective up to 21 days, viable in warm moist soil for more than 1 year.

• Fecal-oral route.

• Humans get infected by: cat feces contact, raw vegetables, gardening, transmission to fetus (if pregnant) - rare in cat. 15-70% of pop. is chronically infected.

• Seropositive cat (already infected before): usually safe, not spreading infection. Only in immunosuppressed → can get new infection, start prod. oocysts again → environment. But, freshly shed oocyst are not infectious immediately. (needs time) → thus directly touching cat does not always cause infetction.

Life cycle: heteroxenous (indirect) but can also be direct (rare, completing its cycle in cats). Predator-prey LC.

• Sylvatic: Wild felids (FH), wild IH

• Domestic: domestic cat, domestic animals as IH

• cats: sexual & asexual development

Pathogenesis and clinical signs: Mild, but severe in immunocompromised.

• Humans: usually no symptoms/mild-flu like illness. Tachyzoites destroys host cells (esp. parenchymal + reticuloendothelial).

  • Prenatal (cong.): abortion/stillbirths, brain damage, hydrocephalus/microcephaly, learning difficulties.

  • Postnatal (after birth-acquired): rare in healthy people. LN infection similar to mononucleosis, local hypersensitivity. 1-2w inc. period.

• cats: most are asymptomatic (infection common, disease rare). Affects young and with weak immune. Common in older (>2y).

  • CS: diarrhea (enteritis), Lymphadenopathy, pneumonia + dyspnea (lungs), encephalitis (brain), retinitis (eye signs)

  • general: fever, weight loss, lethargy.

  • severe cases → can be fatal (weak immune)

• dogs (pigs are similar).

  • Acute: Fever, LN enlarged, nose + eye discharge, pneumonia (common), diarrhea & weight loss.

  • Chronic: Liver (hepatitis), heart (myocarditis), pneumonia, CNS - tremors, ataxia, paralysis.

• Large ru: Abortions, Small ru: abortions, CNS disorders

• Horse, game, poultry: asymptomatic usually

Diagnosis: In cats, finding oocysts in feces can be hard, as eggs are shed before CS. So we use blood tests (serology) & biopsy/body fluids.

Human: Often - combined multiple tests + track Ab levels over time. In acute: high titers of specific lgM and lgA Ab can be seen in the serum, lgG are low. A rise in Ab titer is indicative of active infection, stable high titer of a recent resolving infection and stable low titer of a chronic, latent infection.

Treatment: 

• Cats: Toltrazuril, Clindamycin + trimethoprim.

• Dogs: Sulfonamids + trimetoprim.

• Human: Spiramycin (protect fetus in pregnant). Others: Pyrimethamine + sulfadiazine.

Avoid contact with cat feces, change cat litter daily, avoid raw or undercooked meat. Wash raw fruits and vegetables well before eating. Keep cats indoors to prevent hunting. 

18.Plasmodiidosis of humans and animals.

Classification: Phylum: Alveolata, subphyl: apicomplexa, Class: Haematozoea, order: Haemosporida, fam: plasmodidae, genus: Plasmodium / Malaria

Cause Malaria.

Main species:

• Humans: P. vivax (most common), ovale, falciparum, malariae, knowlesi (zoonotic)

• Monkeys: P. brasilianum, central/south america

• Chimpanzees: P. Scwetzi, africa

Morphology:

Location: Intracellular in RBC, liver cells and macrophages.

Needs two Hosts (all are Heteroxenous):

• FH: Mosquitoes – Anopheles (in mammals)

• IM: Reptiles, birds, rodents, monkey, humans

Geo: Worldwide, but has endemic zones in tropical areas.
Epizoo: causes Malaria. Specific of host and vector. Transmission by insect vector - anopheles mosquito (mammalian).

Life cycle: 1 sexual, 3 asexual stages.

• Gamont (stage) is found in RBCs.

• male form (Microgamont) → makes 8 flagellated microgametes (sperm-like cells).

• After male + female cells join → forms zygote, which can move (Ookinete)

• IH (vertebrate): scizogony/merogony (asexual)

• FH: Gametogony + sporogony

• No sporocyst structure, the sporozoites develop inside oocysts

• RBCs bursts → release of merozoites → triggers feverish malaria attach. (as the parasite flood the blood, releasing waste/toxins)

• Process:

  • Female mosquito bites human, injects sporozoites into blood → goes to liver → enters liver cells (exoerythrocytic stage) → forms schizonts → burst → merozoites

  • Note: P.vivax + P.ovale can sleep in the liver (hypnozoites) - cause relapse later.

  • Merozoites → infect blood cells→ become ring form (trophozoite) → multiplies → burts → release merozoites → fever attacks (malaria paroxysm).

  • Some become gametocytes (sexual forms) → which are taken up by mosquitoes (bites) → fuses and form zygote (ookinete) → becomes oocysts in gul wall → oocyst grows, burst, releases sporozoites, goes to salivary gl. Cycle repeats.

Pathogenesis and clinical signs: Clinical presentation is acute febrile illness, may have periodic febrile paroxysms every 48 – 72 hours with afebrile asymptomatic intervals.

Early symptoms: headache, fatigue, nausea, muscular pains, slight diarrhea, slight fever. Could mistake for influenza or gastrointestinal infection

Clinical signs are anemia, thrombocytopenia, hepatosplenomegaly, renal dysfunction, mental status changes. Prodromal symptoms can range from none to mild to severe, includes malaise, fatigue, headache, muscle pain, nausea, anorexia and flu-like symptoms, marks end of incubation period.

Immunity is acquired, can be transferred from mother to child for 3-6 months.

Infection in monkeys are generally asymptomatic, or cause mild symptoms.

Diagnosis: Stained blood smear, PCR, ELISA, IFAT

Treatment: Mefloquine, Doxycycline, Malarone (also as prophylaxis), Chloroquine, hydroxychloroquine

19. Avian malaria (Hemoproteus, Leucocytozoon, Plasmodium).

This disease is very similar to human malaria, and is transmitted by the bite of infected insects.

Life cycle is also very similar:

-       Merogony occur first in reticuloendothelial system (mononuclear cells) and later in the erythrocytes. 

-       Gametogony and sporogony occur in vectors.

Wide range of symptoms from asymptomatic to drastic decline in population number.

 

Plasmodium

Plasmodium relictum – infect birds all over the world.

Plasmodium gallinaceum

Plasmodium cathemerium 

  (G&C)Highly pathogenic for poultry industry in tropical regions.

Many plasmodium species in birds rarely cause disease in their specific host, but for imported birds cause disease.

P. gallinaceum cause hepato/splenomegaly, anemia and abdominal distension.

Pathogenesis and clinical signs: Plasmodium reproduces in RBC -> bursting of RBC case anemia (birds have nucleus in their RBC), hypoxia, progressive weakness and death. Blood coccidiosis is characterized by intermittend fever, splenomegaly and secondary anemia.

 

Haemoproteus

Haemoproteus meleagridis – Turkey

Haemoproteus nettionis – water poultry

Haemoproteus columbae – pigeon (pigeon malaria)

Intracellular parasites infecting erythrocytes. Called pseudomalaria, due to its similarity to Plasmodium spp.

Transmitted by various biting insects (Culicoides; avian keds (Ornithomyia, Lynchia, Pseudolynchia, Stilbometopa); horse fly (Chrysops)). 

Birds and reptiles as vertebrate host.

Life cycle is similar to Plasmodium. FH infect birds with sporozoites -> merogony in tissues -> merozoites invade RBC and develop into gametocytes, infective stage for FH which ingest them with blood.

Pathogenesis and clinical signs: Subclinical infections, acute form – pigeon. Cause enlarged stomach, enlarged spleen, liver and kidney. They may have a chocolate-brown color due to accumulation of hemozoin. Infected birds may have movement pain, appearance of fluffy feathers, exhaustion, weakness, death, anemia.  

Diagnosis: Finding only gametocytes inside RBC.

Treatment/control: Chloroquine. Control of vectors, insecticides.

Leucocytozoon

Leucocytozoon smithi – Turkey

Leucocytozoon simondi – waterfowl 

Leucocytozoon caulleryi – chicken 

More than 100 species. Parasites of wild birds, but sometimes cause disease in domestic poultry. Located in capillary endothelial cells, RES organs (liver and spleen), leukocytes and erythrocytes.

Vector and FH: Simulium spp.  (black fly -> sporozoites).

Life cycle: similar to Plasmodium spp. Meronts develop in hepatocytes -> formation of merozoites -> enter blood stream -> infect leukocytes -> develop gamont -> ingested by blood-sucking black flies -> gametogony -> develop sporozoites.

Pathogenesis and clinical signs:
5 days after infection cells rupture and there are many schizonts in hepatocytes.
7 days after infection, accumulation of gametocytes in liver, megaloschizons in spleen, lymphatic and other tissue.
12 days after infection, hemorrhagic scars after megaloschizontal rupture. Most infected birds are asymptomatic.
They can show anorexia, anemia, weakness, depression, difficulty breathing and inability to fly, difficult to move, uncoordinated with manifestations of paralysis, granulomatous lesions are visible in the lungs, heart, brain and peripheral nerves. Young birds die within 24h. They acquire immunity after overcoming the disease, and adult birds are reservoirs.

Diagnosis: finding gametocytes in microscopic examination of stained blood smears. They are large, lack pigment and distort the RBC and WBC, making it no longer identifiable. Histopathological examination of the liver, spleen and brain with finding of megaschizonts. Pathological anatomical autopsy, enlargement of liver and spleen

Treatment: Therapy is usually not effective. We can give pyrimethamine, sulfadimethoxin and clopidol in feed. Vector control is important. Can use anti-Leucocytozoonous vaccine when parasitemia is reduced but infection is not obvious. 

20. Babesiosis in ruminants and horses.

Phylum: Alveolata

Subphylum: Apicomplexa

Class: Haenatozoea

Order: Piroplasmida

Family: Babesiidae

Genus: Babesia

Main species:

B. bovis – Texas cattle fever. Small

B. bigemina – Texas cattle fever. Large

- Affect vary of ruminants. Deer, water buffalo, zebu and cattle cam be infected

-  Vector – boophilus anulatus

-   OIE-listed

B. divergens – cattle. Small.

B. major – cattle. Large

B. ovata – cattle 

B.equi - horses

B. caballi - horse, donkey

Morphology: Pyriform, round and oval shape, can be small (1-2um) or large (2-5um). Large babesia is located in the central of blood cells, paires pyriform shape. Small babesia is found in the periphery of the cells, as single ring form. Free sporozoite, no sporocyst.

Location: Intracellular parasite, found in erythrocytes, lymphocytes, histiocytes and erythroblasts.

FH: Ticks

IM: Vertebrates, infect all cattle and domestic animals

Geographical distribution: Worldwide
Epizootology: Transmission by vectors. B. bigemina – Boophilus annulatus. Transstadial and transovarial transmission. Zoonotic: B. divergens, B. bigemina, B. equi, B. microti

Life cycle: FH and vectors – sexual reproduction (gametogony and sporogony). IM – asexual reproduction

Sporozoits are passed into the blood of IH by ticks taking a blood meal. They invade blood cells and go through merogony -> merozoits can affect new cells or develop into gametocytes, taken up by FH during feeding Inside FH they go through Gametogony -> kinete. Ookinete go to the eggs and  transmit transovarially to next generation, so all stages of the tick will potiantially be infective OR it can transmit transstadial -> sporogony in mouth of tick.

Pathogenesis and clinical signs:
B. bigemina: appear 2-3 weeks after tick infestation. Infection period 4 - 5 days. Cause anorexia, hemoglobinuria and fever up to 41.5C. Animals may separate from the herd, stand with an arched back and display a roughened coat, dyspnea and tachycardia. At the start of an infection, red mucous membranes and then they become pale -> anemia, often develops rapidly and cause hemoglobinuria and hemoglobinemia.
B. bovis takes slightly longer. Infection period 10 - 12(?). More virulent. Similar clinical signs, but they usually develop a higher fever, anorexia, depression, ataxia and circulatory shock. Hemoglobinuria and hemoglobinemia are less common. Infected erythrocyte in brain capillaries may result in incoordination, teeth grinding and mania. Animals may be found on the ground with the involuntary movements of the legs. Death often follows CNS signs. Can form post-mortem lesions.

More severe in adult cattle than calves. Mortality in untreated adult cattle is 50-90%. Cattle that recover is usually immune for life.

B. equi: Fever, hemolytic anemia and jaundice. Incubation 8 - 10 days, disease last for 10 days. Death may occur during first 24 - 48h.

Diagnosis: Stained blood smear or serology. Post mortem lesions in brain capillaries.

Treatment:Diminazine, tick control, regular dipping of cattle, vaccines.

21.dog piroplasmosis (Babesia, Hepatozoon).

Main species, morphology and epidemiology:

Species and vector ticks of LARGE babesia (2-5 μm)

Babesia canis canis- Dermacentor reticulatus (Europe, Asia)

Babesia canis vogeli- Rhipicephalus sanguineus Less pathogenic!

-  Often without clinical signs, but fatal in puppies

Babesia canis rossi - Haemaphysalis leachi Most pathogenic! (South-Africa)

Pyriform organisms, pear-form in RBC.

 Species and vector ticks of SMALL babesia (1-2 μm)

Babesia canis gibsoni - Rhipicephalus (Europe, Africa, Asia, America)

Single form organisms

Geographical distribution: Worldwide, but data relation to European infection have mostly been collected

Life cycle: Same as in cattle

Pathogenesis and clinical signs: Babesia canis (young dogs), Babesia gibsoni (all ages).

Babesia parasite is transmitted to the dog 2-3 days after attachment of the tick → infective sporozoites migrate from the tick’s salivary gland to the host’s blood.

Obligate intracellular parasites that invade, divide within and rupture RBCs → direct parasite-induced RBC damage. Causes ischemia (hypoxic damage – RBCs cannot transport O2).

Clinical symptoms are lack of energy and appetite, pale gums, fever, enlarged abdomen, colored urine, icterus, weight loss and discolored feces.

Acute form: general findings (fever, weakness, pale mucus membranes, depression).

Chronic form: irregular temp, variable appetite, loss of condition. Dogs are permanent carriers after infection. Brain necrosis post mortem.

Diagnosis: Examination of stained blood films – easiest (Giems-romanowski staining, Diff-quick, pappenheim). Serology only show exposure. Must utilize clinical data to distinguish infection from disease. Blood smear examination is useful for clinical babesiosis in dogs. However, the sensitivity of this method is very low. 

Treatment: Preparations with active substance imidocarb at dose of 2-5mg/kg. Can also use diminiazen-diaceturate and trypan blue. Symptomatic therapy. Tick control, tablets, collars, sprays, shampoo.

Phylum: Alveolata

Subphylum: Apicomplexa

Class: Haenatozoea

Order: Adeleida

Family: Hepatozoidae

Genus: Hepatozoon

Main species: Hepatozoon canis (old world), H. Americanum (new)

Morphology: It is more elongated.

Location: Gametocytes in circulating leukocytes and tissue “cysts” in muscle.

FH: Rhipicephalus sanguineus (old world), Amlyoma maculatum (new world)

IM: Dogs

Geographical distribution: Common in South and North-America
Epizootology: Trick-transmitted by ingestion.

Life cycle:  Dog ingest cysts, sporozoits release in GIT, they migrate by blood or lymph to muscles, spleen, liver, lymph nodes and bone marrow. Here they go through merogony. In muscle tissue, they can form cysts in which merogony occurs within. Meront rupture and merozoites are released. This caused inflammatory response, recruiting neutrophils and monocytes. The merozoits can repeat the asexual cycle or invade these leukocytes and develop into gametocytes, which is infective for feeding ticks -> Gametogony and sporogony. Dog ingest tick.  Merozoites in WBC can also cause intrauterine transmission to puppies.

Pathogenesis and clinical signs: Clinical signs are fever, lymphadenopathy, ocular and nasal discharge, anorexia, cachexia, anemia, leukocytosis, paraparesis, depression, muscular hyperesthesia and a reluctance to move. The animal may develop severe cachexia, vasculitis and renal failure. Cysts containing merozoites may be found in muscle biopsies. Leukocytes may contain gametocytes.

Diagnosis: By blood smear, detection of merozoites in neutrophils and muscle biopsy.

Treatment:Dimazene aceturate, imidocarb diproprionate, tetracycline, doxycycline, toltrazuril. 

22.Theileriidosis of mammals.

Phylum: Alveolata

Subphylum: Apicomplexa

Class: Haenatozoea

Order: Piroplasmida

Family: Theileriidae

Genus: Theileria

Main species:

Theileria parva parva – East coast fever (bw cattle)

T. parva bovis – bw cattle

T. parva lawrencei – buffalo to cattle

T. annulata – Tropical theileriosis/ Mediiterranean theileriosis

T. lestoquiardi – sheep and goat, can have 100% mortality.

T. equi

Morphology:  

Location: Found in predominantly in lymphocytes, where development occurs. Can be found in RBC-

Vector/FH: Ticks. Riphicephalus appendiulatus (T. parva), Hyalomma anticolicum (T. lestoquiardi) T. annulata – hylomma spp.

IM: Ruminants

Geographical distribution: T. annulata in North-afrida, mediterreanean costal area, middle east, india, and Asia.
Epizootology: Transstadial transmission by ticks (bw generations)

Life cycle: T. parva life cycle

IH – sporozoits are relased from the tick during feeding on a vertebrate host. The sporozoits become trophozoits, attach to the lymphocytes and enter by “zippering” mechanism and develop into merozoits. Merozoits multiply inside the lymphocyte (merogony) and the cell ruptures releasing merozoits to infect red blood cells and become piroplasms and are infective to ticks. They don’t multiply in RBC.

FH – tick larvae and nymphs are infected when they suck blood from an infected vertebrate IM. Piroplasm -> gametes and form a zygote, which develop into a kinete. Kinete travels to salivary glands where it will undergo sporogony and can infect new IM hosts during feeding. 

Pathogenesis and clinical signs: T. parva. Enlarged, hemorrhagic and edematous lymph nodes. Just before death, a sharp fall in body temperature is usual, and pulmonary exudate pours from the nostrils. Death within 2-4 weeks. Necropsy show edema of lungs, hyperemia, infarcts, thrombosis and lymphoid hyperplasia in spleen.

T. annulata cause mortality up to 90%. Characteristic signs include fever, swollen superficial lymph nodes. Rapid loss of condition and hemoglobinuria. Morphologically similar to T. parva. There are many other species known to occur in wild ruminants that can be mixed and complicate the diagnosis of T. parva.

Diagnosis of T. parva: demonstration of parasite in Giemsa-stained blood, lymph node and tissue impression smears. But it is difficult to differentiate between schizonts and piroplasms of different Theilieria species. IFA test is better (detection of antibodies), PCR and probing. Can be mixed infection of different species, which complicate the diagnosis of T. parva.

Treatment:T. parva.Parvaquone and its derivate buparvaquone, halofuginone. Treatment with these is highly effective when applied in early stages, less effective in advanced staged. Incidences can be reduced by tick control.

23.Balantidiosis of pigs.

Phylum: Ciliphora

Class: Litostomatea

Order: Vestibulferida

Family: Balantidae (only one genus)

Genus: Balantidium

A worldwide common parasite found in intestinal tract of domestic pigs and wild boars. It lives in the opportunistic protozoa of the large intestine of most pigs.

Main species: Balantidiu coli

Morphology: Nuclear dimorphism = 2 nuclei: micronuclei and macronuclei. Macronucleus is typically elongated and kidney-shaped, micronucleus is spherical. Moves with cilia. The cyst is round or oval. Transparent. 2 prominent contractile vacuoles, indicating osmoregulation. Large size.

Has 2 forms:

· Infective cyst: Encapsulated form, non-mobile, but survives in environment.

· Trophozoite: Found in cecal area and throughout large intestine.

Location: Large intestine

FH: Pigs, wild boar and sometimes humans.

Geographical distribution: Found most often in tropical regions throughout the world.
Epizootology: Not a common human disease, less than 1% infection rate. 20-100% in pigs. Fecal-oral transmission.

Life cycle: Oral ingestion of cyst -> trophozoite hatch in small intestine -> move and settle down in large intestine, where it feeds on bacteria and starch, or by invading the mucosal wall of the large intestine. Here they secrete a substance that destroys intestinal tissue and creates ulcers or abscesses.

Trophozoites multiply asexually (binary fission) or sexually (conjugation) -> form new cysts -> excreted in feces. Cyst can live in environment for months. Trophozoite can also be shed in feces but they disintegrate quickly in the environment.

Pathogenesis and clinical signs: Due to low virulence -> pigs are usually asymptomatic.

Trophozoites rarely invade the intestinal wall cause haemorrhagic diarrhea, lesions and ulcers of intestine.

Diagnosis: Flotation method. In acute diarrhea -> motile trophozoites are seen in direct smears. Trophozites are large and they only parasitite humans and pigs that have cilia. Infection may disappear spontaneously or the host may become asymptomatic and be carriers.

Treatment: Metronidazole, Tetracycline.

24.Encephalitozoonosis and Nosematosis

Phylum: Microsporidia

They are small, unicellular, spore-forming parasitic fungi with obligate intracellular development.

Main species: Encephalitozoon cuniculi

Morphology: Very small. The wall consists of an endospore and an exospore, enclosing the cytoplasm. Cytoplasm include 1 or 2 nuclei, a vacuole and an extrusion apparatus. No mitochondria. Polar tubule - coiled organelle that injects spore content into host cell.

Location: Unknown, but affects CNS and kidneys

FH: Rabbits. Can infect humans.

Geographical distribution:
Epizootology: Oral or transplacental transmission. Endemic in captive and wild rabbit populations. Can be zoonotic! Opportunistic in immunocompromised patients with aids.

Life cycle: Infective form is the resistant spore. It is ingested or inhaled by rabbits. It uses its polar tubule to penetrate host cells and injects infective sporoplasm. Sporoplasm divides through merogony -> merozoites undergo sporogony -> sporonts -> sporoblasts -> spore. Spores increase in number and when cytoplasm is completely filled they released by the host cell. These spores can infect new cells, continuing the cycle, or they can be shed in feces or urine.

Pathogenesis and clinical signs: Merogony: microsporidia does not cause serious cell damage.

Sporogony: cause cell destruction and focal granulomatous inflammation of surrounding tissue. Immunosuppressed host may suffer serious disease with fatal outcome. Can cause keratoconjuctivitis, infection of respiratory and urogenital tract

Rabbits: Spread via blood to kidneys and brain. Clinical signs are head tilt, kidney lesions, damage to CNS, nonspecific neurological signs. Usually asymptomatic, but rabbits may develop mild, chronic renal disease. Some develop brain lesions -> head tilt, convulsions, tremors.

Diagnosis: Light microscopic examination of stained fecal samples, identification of spore in feces. Transmission electron microscopy is standard and necessary to identify the species. IFA and PCR is also used.

Treatment: Fenbendazole, fumagiline, nitazoxanide. 

(MÅ TA MED NOSE GREIA)