PARASITOLOGY

pre-patent period: The interval between infection of an individual by a parasitic organism

and the first ability to detect from that host a diagnostic stage of the organism.

viviparous: Zygote has a development inside a specialised matrice to receive nutrients.

Ovoviviparous: producing eggs that are hatched within the body, so that the young are
born alive but without placental attachment, as certain reptiles or fishes.

General parasitology

Study of the relationship between a parasite and its host

Parasites – parasitism
Parasites are organisms that use as source of food and habitat another organism, he lives
in/on another organism (= host)
• Host: usually larger, harbors the parasitic species
• Parasites: smaller, obtains food and habitat from host

The parasite

 LOCATION ON THE HOST

 Ectoparasite (infestation)
Lives on the surface of the body of the host
Fleas, lice, ticks, mites…

 Endoparasites (infection)
Lives within the host
Roundworms, tapeworms, whipworms…

 AMOUNT OF TIME ON THE HOST

 Temporary
Short period of time: visit just for food
Ticks, mosquitoes, fleas...

 Stationary
Spends definite period of time in/on the host
Most of the parasites

Can be:
- Periodic: leaves host to complete development
- Permanent: all stages are developing within the host, entire life
Mites, lice, piroplasms…
  NUMBER OF HOST
- Monoxenous: one host
- Dixenous: two hosts
- Trixenous: three hosts

 TYPES OF PARASITISM
 Facultative
Free living organism that can become parasitic in certain host, certain conditions
Green bottle fly

 Obligatory
Temporary
Stationary

 PARTICULAR FORMS OF PARASITISM

 Erratic parasitism
Aberrant parasite
Seen in unusual locations in host
Ascaris suum: normally small intestine but aberrant in stomach, liver

 Hyperparasitism
Parasite within a parasite
Piroplasm in tick (Babesia), tapeworm larvae in fleas…
 Accidental parasitism
Appears in unusual host
Heartworms in man

The host of parasite

DEFINITIVE HOST
In which the parasite reaches sexual maturity and reproduces
Harbors adult parasite / gametogonic stages for protozoans
Ticks are DH for piroplasm
Dogs are DH for heartworm

INTERMEDIATE HOST
Immature parasitic stages undergo development in this host
Larval stages / asexual stages of protozoa
Heartworm larva in mosquitoes

OTHER TYPES OF HOST

Paratenic or transport host
No parasite development, but he continues to live and is infective to next host
Paratenic host serves as a transport host
Final host must eat this host for adult parasite to develop
Reservoir host
Animals that serve as source of infection to human

VECTORS
Transmit parasites from host to host
Biological vector
Essential in life-cycle of parasite

Mechanical vector
Unessential in life-cycle of parasite (phoretic)

Host contamination SOME EXEMPLE

 Direct contact
Often in ectoparasites
Due to their mobility and biological particularities

 Indirect
Through the objects with parasite stages
Beds

- Orally
The majority of gastrointestinal, tissular parasites
Involves infesting of infectant stages (eggs, larvae)
Food or water contamination

- Galactogenic transmissions
Through the milk

- Mucosal
Genital
Nasal
Conjunctival mucosa

- Transplacental
Some systemic parasitosis
In larvae of nematodes
May cause life-threatening disease

- Trans-cutaneous
By ectoparasite vectors: Babesia, Leishmania
Nematode larvae

- Transovarian
Babesia in ticks
  PARASITE TRANSMISSION
 How parasites transfer from one host to another
- Passive
Parasite doesn’t travel to host
Usually ingested
Roundworms
- Active
Parasite travels to host
Fleas
- Inoculative
Other organisms inject parasite into the host
Called “vector”
Often takes blood from DH and has sucking mouthpart
Mosquitoes, ticks

 DISEASE VECTORS
- Mosquitoes
Heartworm disease

- Sand flies (Phleobotominae)

Leishmaniosis

- Ticks
Bebesiosis
Theileriosis

Life cycles of parasites

Entire sequence of stages in the life of a parasite
Parasite may be species specific: affect only 1 species of host (Lice)

Direct life cycle

Parasite transfers from one host to another host of same specie
No intermediate host
Whipworms, ascarids

Indirect life cycle

Parasite requires at least one intermediate host to complete its life cyle
IH harbors immature parasite
DH harbords adult parasite
Heartworms, all tapeworms

 MIGRATION OF PARASITES
Route followed by parasites from the contamination site reaching the target organ/tissue,
but with important development changes on this route

Migratory parasites
With complete or incomplete migration
Non-migratory parasites
Changes don’t occur on the route

Parasites infection involves 2 stages :

a) Prepatent phase
Period for development of preimaginal stages

b) Patent phase
Maturity of adult is acquired

The consequences of the host-parasite relationship

Adaptation of parasites for the parasitic life

Morphological adaptations:
Body shape
Ectoparasites: flattened dorso-ventrally (lice) or latero-lateral (fleas)
Endoparasites: the body is flattened (trematode/cestode), cylindrical (nematode), piriform

Body size
From few micrometers to meters

Body pigmentation
Specific to endoparasites: brown (bed bugs), brownish gray or reddish

Locomotion organs
Ectoparasites: specialized

Attaching structures
Suckers, chaetae

Digestive system
Very developed for temporary parasites
Mouthparts: specialized in ectoparasites

Nutrition
By osmosis in protozoan
Reproduction
Genital apparatus very developed
Hermaphroditic in trematodes, cestodes

The actions of the parasites on the host – Pathogenesis

Mechanical action
Important for large and migratory parasites
Expressed as:
- Intestinal occlusions/obstruction
 - Irritation
- Compression and atrophy
- Spoliator action
- Direct: due to consumption of
- Nutrient of the host (cestodes)
- Blood (ticks)

Indirect
- Selective consumption
- Disturbing host metabolism
- Toxic action
One of the major parasitic aggression due to:
- Exotoxins
- Endotoxins
Effect:
- Anticoagulant and hemolytic (ticks)
- Neurotropic (paralysis, allergic)
- Anemia
- Inflammatory (especially if reinfection)
- Circulatory disorders (hypotension, bradycardia)

Inoculative action
More common in:
Hematophagous ectoparasites (ticks, mosquitoes)
Migratory / non-migratory endoparasites

The actions of parasites are influenced by:

 Intensivity
Denotes the number of individuals of a parasitic species present in/on the host
 Exentsivity
Number of infected individuals from a given host population
Expressed as percentage

Reactivity / reaction of the host

Reactivity of the celllular subsystem

 Phagocytosis
 Hypereosinophilia
 Celullar hypertrophy

Reactivity of the tissular subsystem

 Tissue atrophy : in metacestodes
 Encapsulation : parasitic granulomas
 Inflammation
 Neoplasia

Reactivity of the humoral subsystem

Immunity:
- Natural
- Acquired (natural infection, post vaccinal)
- Sterile (do not allow the parasites to develop)
- Non-sterile (premunition): in babesiosis (the parasite is still present in the body but at
very low level, the animal won’t dvp the disease)
Host immune response alteration may occur resulting some syndrome harmful to the host:
Hypersensitivity (anaphylaxis in hydatidosis, allergy in dermatitis)
Immunodeficiency

Taxonomy
Kindgom/ Phylum/ Class/ Order/ Family/ Genus/ Species
Kingdom ANIMALIA:
Phylum Platyhelminthes: flatworms
Phylum Nemathelminthes: cilindrical worms
Phylum Arthropoda: arthropods

Parasitic diseases
Construction of disease names by adding “-osis” to the stem of the name of the parasite
taxon
Fasciola = fasciolosis
Ascaris = ascariosis
Trichinella = trichinellosis…
Some diseases names are not derived from the taxonomic name of the parasites:
Sleeping sickness
Malaria
Myasis…
Epidemiological importance: some parasitic diseases are zoonoses (toxoplasmosis,
trichinellosis…)

Control of parasitic diseases

Measurements that aim to reduce the frequency and the intensity of parasitic infection
It’s not necessary to have the animal free of parasites
immunity)
Management (general) Nonspecific action :
External: improper the environment for the developlent of parasites
Internal / in the barn / shelter: maintaining the hygiene
Providing a complete diet (nutrients)
Selecting animals resistant

Biological measures
- Using immune sera or hyperimmune
- Use of vaccines
- Use of natural predators of parasites, or of their larvae stages
- Use of substances with similar action of growth hormones
Controlling the intermediate host

Medical measures :
Use of specific antiparasitic medication, respecting the principles to prevent and avoid
development of chemoresistance

II – Parasitic disease
KINGDOM PROTISTA
PHYLUM PROTOZA – Protozooses
General characteristics:
Morphology
Unicellular eukaryotes
Most are motile (flagella, cilia, pseudopodia)
Free living

Biological form
Trophozoite: stage of the protozoa in the host which feeds and grows
Cysts / oocysts / spores: resistance forms / spreading

Nutrition
Osmosis
Phagocytosis

Reproduction
Asexual
Fission: cell divide in 2 daughters cells
Internal budding
Schizogony: multiple fission
Sexual
Gametogony
Conjugation
Both

SUBPHYLUM SARCOMASTIGOPHORA - Sarcomastigophoroses

Class Sarcodina / Order Amoebida / Family Entamoebidae / Genus Entamoeba

► AMOEBIASIS
Entamoeba hystolitica
Etiology:
- Parasite in the intestine of human beings, but also dogs and cats
- Inhibits the mucous and sub-mucous layers of large intestine

Direct life cycle

Exists in 2 forms:
Magna or trophozoite (bigger)
Pathogenic
Can produce ulcers, abscesses
Minuta or precystic
Non-pathogenic
Can undergoes encystations and helps the transmission of parasites
Cysts
Passed in the feces of infected humans
Infective stage

Epidemiology:
- Parasites of humans which serve as reservoir for animal infections
- Source of parasites
- Cysts are often shed by asymptomatic carriers
- Cysts are resistant to environmental insults
- Survive in water, soils, food
- Killed by heat
- Risk factor
- Poor hygiene
- Contamination
- Oral through water, food, hands

Pathogenesis:
- Feed mainly on the tissues of the intestinal wall and often produces severe ulcers and
abscesses
- In chronic cases, it may enter the blood circulation to reach the liver, lungs, brain
- Intestinal
- Ulcer formation: flask-shaped ulcers
- Leads to bloody diarrhea
- Extra-intestinal
- Spread from intestine
- Occasionally trophozoites enter the bloodstream
- Transported to the liver (hepatic amebiasis)

Clinical signs:
- Stress aggravates the signs
- Diarrhea is the classic one
- Fluid losses
- Dehydration
- Cramps…
- GI perforation and peritonitis
In dogs
Usual chronic
Diarrhea
Swine and guinea pigs
Usually non-clinical

Diagnostic:
 - Clinical signs
- Epidemiology
- Examination
- Fecal smear
- Flotation
- Culture
- Trophozoites in fresh fecal smear
- Cyst in formed feces
- Necropsy

Treatment:
- Intestinal infection
- Nitroimidazole derivatives
- Metronidazole

Control:
- Prevent fecal contamination of food and water

SUBPHYLUM SARCOMASTIGOPHORA
Class Sarcodina / Order Amoebida / Family Entamoebidae / Genus Malpighamoeba

► MALPIGHAMOEBOSIS
Malpighamoeba mellificae

Parasitic disease of honey-bees, occuring mainly on spring, characterized by diarrheic

syndrom, weakness and shortening the lifespan of infected bees

Etiology and epidemiology:

Parasite in the Malpighian tubule and midgut of adult bees
2 forms: trophozoites and cyst

Contamination
- Oral
- After ingestion the cyst germinate and migrate to the Malpighan tubule
 - Result in trophozoites, multiply and destroy the epithelium
- After 3-4 weeks, result cyst and eliminate

Clinical signs:
Often found with nosemosis: more severe, high mortality

Lesions
Malpighi tubules are thickened, transparent and structures of the cells are destroyed

Diagnostic:
Microscopic exam to detect cyst in the feces of the bees

Treatment and control:

- Neotektin
- Good hygiene

SUBPHYLUM SARCOMASTIGOPHORA
Class Mastigophora – Flagellates

GENERAL FEATURES
Morphology
- One or more flagella
- Trophozoite
- Cyst (only some)
- Various structures:
- Undulating membrane with attached flagellum
- Kinetosome that gives rise to the flagellum
- Axostyle for body support

Hemoflagellates
Blood and tissue flagellates

Mucosoflagellates
Intestinal and reproductive flagellates
Direct life cycle

Order Kinetoplastida / Suborder Trypanosomatida (HEMOFLAGELLATES)

General characteristics:
One flagellum (free or attached)
Golgi present near flagellar depression
Family Trypanosomidae
Trypanosomes and Leishmanids
Heteroxenous and some monoxenous
Found in blood or tissue cells of vertebrates
Most use blood-sucking intervertebrate vectors
Trypanosomes transmitted variously depending on species
Blood sucking flies
Fleas
Biting flies
Venereal
- Morphology: 4 TYPES:
- Amastigote: in tissue
- Promastigote: in gut of vector
- Epimastigote: in gut of vector
- Trypomastigote: in blood
- Trypanosoma spp.: all 4 morphologies can be found
- Leishmania: amastigote is predominant / promastigote in vector

Genus Trypanosome
Based on site of development and method of transmission:
Salivaria (anterior station)
Develop in front portion of vector’s digestive tract
Transmitter via salivary gland through saliva and biting

Stercoraria
Develop in hingut
Transmission via feces

► CHAGAS’ DISEASE
Trypanosoma cruzi
Concerns dogs, humans, cats, racoon, opossum…
Transmitted by reduviid true bugs (ingestion of bug and/or feces)

Trypanosoma brucei
T. Brucei brucei
Cause NAGANA
Transmitted by Tsetse fly
Salivaria
Infect domestic animal and wild ruminant (pathogenic in domestic rum.)
T. Brucei Gambiense and T. Brucei rhodesiense
Infect human
Transmitted by Tsetse fly
Cause AFRICAN SLEEPING SICKNESS
► DOURINE
Trypanosoma equiperdum
Most important veneral disease in horses, responsible for great losses whenever it occurs

Morphology:
- Polymorphic
- Undulating membrane and small kinetoplast
- Big round nucleus with granular cytoplasm

Epidemiology:
- Contamination
Sexual transmission
Only trypanosome without vector
- Source of infection
Infected animals
Occurs also in donkeys but asymptomatic

Pathogenesis:
 Due to rapid multiplication
 Exacerbation, tolerance or relapse
 Pyrexia
 Tumefaction and local edema of the genitalia and mammary glands
 Incoordination and facial paralysis
 Ocular lesions, anemia, emaciation…

Clinical signs:
Chronic form
 First phase: inflammation of the genitalia
Swelling of the genitalia
Circumscribed areas of the mucosa of vulva or penis
Fever
  Second phase: cutaneous lesions
Circular, flattened plaques
 Third phase: nervous disorders
Muscular paralysis
Incoordination and compete paralysis
Emaciation, fever…

Diagnosis:
- Clinical signs are relevant only for the 1st and 3rd phase
- Serologic
- Parasitological

Treatment and control:

Under veterinary surveillance

► LEISHMANIOSIS
Leishmania
Severe zoonotic disease
The most important etiological agent of canine leishmaniosis: Leishmania infantum, dogs are
the main peri-domestic reservoir
Etiology:
Leishmania tropica
Cutaneous leishmania
Leishmania brasiliensis
Cutaneous leishmania
Leishmania donovani
Visceral leishmania : Dum Dum fever
Transmitted by sandflies: Phlebotomus spp.

Morphology:
- Amastigotes
- Promastigotes

Epidemiology:
- Seen in rural areas
- Mediterranean region
Clinical signs (in dogs):
- Lymphadenopathy
 - Dermatitis
- Alopecia
- Skin, lips and eyelids ulcers
- Fever
- Cachexia
- Hepato-splenomegaly…

Pathogenesis:
- Macrophages and reticuloendothelial cells infected first
- Favorite tissues: spleen and liver
- Fibrosis develops

Diagnosis:
- Amastigotes in tissue biopsy
- Lymph nodes
- Bone marrow
- Blood
- Liver
- Spleen
- Culture
- Necropsy

Treatment:
- Complex, long time, no complete cure
- Pentavalent antimonial

► CUTANEOUS LEISHMANIASIS
Leishmania mexicana
Transmitted by Lutzomyia sp.
Forest zoonisis in dogs, tapirs, rodents and other wild mammals
Lesions on ears, face and nose

SUBPHYLUM SARCOMASTIGOPHORA
Class Mastigophora – Flagellates / Order Trichomonadida / Family Trichomonadidae

►TRICHOMONOSIS
Trichomonas fetus
Bovine genital trichomonosis
Etiology:

In cattle: uterus, prepuce

Trophozoites only
Sexual transmission

Epidemiology:
- Common in herds with natural service
 - Spread by infected bulls
- Bulls remains infected and serve as permanent carriers
- No immunity development
- Cows develop immunity
- Some cows can be carriers and give normal birth

Pathogenesis:
Bulls: little
Cows:
- Vaginitis
- Trophs invade uterus: cervicitis, endometritis, pyometra
- Fetus attacked about 7 weeks of gestation
- Abortion
- Can lead to infertility and poor conception rate

Clinical signs:
- Vaginal discharge
- Early abortions
- Repeated irregular estrus periods after abortion

Diagnosis:
- Clinical history
- Direct exam for the presence of motile organisms:
- Vaginal secretions
- Uterine washing fluids
- Fetal fluids
- Culture

Treatment:
- Metronidazole
- Dimetridazole

Control:
- Use young bulls: < 3y
- Use artificial insemination
- Give cows at least 90days sexual rest
 ► DIGESTIVE TRICHOMONOSIS

In piglets: In poultry: In dogs: In cats: In equine:

Trichomoncas suis Trichomonas gallinae T. canistomae T. fellistomae T. equi
GI tract Morphology: Mouth Mouth GI tract, cecum, colon
T. buttreyi - Trophozoites Can cause: Can cause: T. fecalls
Cecum, colon - 4 anterior stomatitis, stomatitis,gingivitis Cecum, colon
T. rotunda flagellums gingivitis
Cecum, colon - Thick axostyle
Life cycle:
- Direct
- Contamined water
- Regurgitative feeding
- Carnivorism by raptors
- Can survive 20mn in water and up to 5 days in moist grain

Epidemiology:
- Turkeys and chickens are infected through drinking contamined water
- Older birds serve as reservoir
- Recovered birds are immune but act as asymptomatic carriers

Pathogenesis:
- In doves and pigeons (youngs)
- Caseous necrotic masses in upper digestive tract
- Acute lesions in mouth, pharynx, oesophagus and crop
- Inflammation and creamy white exudate on the mucosa
- Chronic: mucosa lesion becomes yellow and larger, may invade the sinuses, beak &
eyes

Clinical signs:
- Depression
- Salivation
- Emaciated
- Respiratory distress and exhibit open mouth
- Difficulty closing the mouth, eating, drinking
- Watery eyes
- Diarrhea…

Diagnosis:
- Clinic signs and characteristics lesions
- Confirmatory:
- Identify motile trichomonads

Treatment:
- Only with captive birds
- Nitroimidazole compounds
► HISTOMONOSIS – THE BLACK HEAD DISEASE
Histomonas meleagridis
Characterized by necrotizing lesions affecting the liver and the caeca
Etiology:
- Morphology
 Polymorphic flagellate
 Trophozoite (larger vegetative form)
 Amoebic trophozoite stages with pseudopodia
 3rd type of relatively small and rounded parasitic cells:
 Present in the excrements of the birds and the eggs of nematodes

Epidemiology:
- Susceptible species are turkeys, chickens, faisants…
- Main vector is Heterakis gallinarum through eggs

Pathogenesis:
- Inflammatory reactions
- Cytohistolitic actions
- Lesions caused:
- Typhlitis with fibrinous content
- Foci of necrosis in the liver

Clincal signs:
- Sulfur yellow coloured feces
- Depression
- Blackening of the skin of the head (cyanosis)

Diagnosis:
- Clinical signs
- Necropsy

Treatment:
- Similar as trichomonosis

SUBPHYLUM SARCOMASTIGOPHORA
Class Mastigophora – Flagellates / Order Diplomonadida / Family Hexamitidae

► GIARDIOSIS
Giarda
Morphology:
- Trophozoite
- Small intestine and diarrhea
- Ventral sucking disk
- 8 flagella
- Cyst
- Resistant for environmental transmission
- Found in formed feces
Epidemiology:
- Cyst found in water
- Asymptomatic carriers that shed cysts are common
- Giarda duodenalis infection common in dogs

Pathogenesis:
- Throphozoites attach the surface of enterocytes in the small intestine
- Caused damage to enterocytes (functional changes: malabsorption, maldigestion)

Clinical signs:
- Incubation period for acute disease 1-2 weeks
- Diarrhea
- Malodorous, gray, voluminous
- Increased mucous
- Not hemorrhagic
- Flatulence

Diagnosis:
- Trophs in diarrhea
- Cysts formed or semisolid feces
- Fecal exams

Treatment:
- Metronidazole

Control:
- Hygiene
- Treatment
- Disinfect environment