Toxoplasmosis
Overview
Introduction
Etiology
Epidemiology
Gross lesions
Microscopic lesions
Diagnosis
Pathogenesis
Differential Diagnosis
Clinical signs
Introduction
• Toxoplasmosis is an infectious protozoal disease of many species of mammals
and birds.
• Characterized clinically by abortion and stillbirths in pregnant ewes and in all
species by encephalitis, pneumonia and neonatal mortality.
• An important zoonotic disease having world wide distribution.
Etiology
scientific classification
Phylum
●
●
Apicomplexa
Toxoplasma gondii
Name derived from “toxon” meaning arc or bow
Family
Sarcocystidae
(curved shape of Tachyzoites)
●
Obligate intracellular protozoan parasite
●
Has three morphological forms.
Sub family
Genus
Toxoplasmatinae
Toxoplasma
Etiology
Asexual
Tachyzoites (or endozoites)
Sexual
Bradyzoites (or cystozoites)
•
Obligate intracellular
form
•
Encysted form
•
Crescent shaped form
with a central nucleus
•
Resist digestive
enzymes
•
Multiplies rapidly
•
Multiply slowly
•
Seen in acute infection
•
Characteristic of chronic
infection
1 sporulated oocyst contains 2 sporoblast.
Each sporoblast contains 4 sporozoites
Oocyst
•
•
Shed in feline
feces
Takes 1-5 days
to sporulate and
become infective
Etiology
Fig: Tissue cysts of T. gondii in mouse brains.
A)
Tissue cyst with three bradyzoites, each with a terminal nucleus (arrows).
Note the thin cyst wall (arrowhead)
B)
Three tissue cysts with well-defined cyst walls (arrowheads).
C)
Intracellular tissue cyst in section. Note the thin cyst wall (arrow) and the host
cell nucleus (arrowhead). H & E stain.
Fig: Tachyzoites of T. gondii. A dividing tachyzoite
(arrowheads) and single tachyzoites (arrows).
Impression smear feline lung, stained with Giemsa
stain.
Fig: Oocysts of T. gondii. (A) Unsporulated oocyst. Note the central mass
(sporont) occupying most of the oocyst. (B) Sporulated oocyst with two
sporocysts. Four sporozoites (arrows) are visible in one of the sporocysts
Epidemiology
Hosts
•
Felines are only definitive host
•
Infections can occur in a wide range of vertebrate intermediate
hosts (including humans)
Transmission
Oral route:
Ingestion of sporulated oocysts contaminated soil, food or water
Ingestion of tissue cyst containing bradyzoites
Transplacental transmission
Laboratory accidents
Pathogenesis
Has two developmental cycle:
Enteroepithelial cycle and extraintestinal
cycle
Enteroepithelial cycle occurs in cat while
extraintestinal cycle mostly occurs in extraintestinal tissue of non-feline species like
mammal and avian host but may also occur
in cat
Pathogenesis
Ingestion of sporulated
oocyst or tissue
containing bradyzoites
by cat
Oocysts (Unsporulated)
are discharged from
epithelial cells and are
discharged along with
feces.
(Enteroepithelial cycle)
Cyst rupture, release large
no. of Bradyzoites which
enter intestinal epithelial
cells
Oocyst form in epithelial
cells of small intestine
after fusion of gametes
Bradyzoite undergo
various multiplicative
stages (A, B,C,D,E) or
schizogony.
After few schizogony, Type E
produces male and female
gametes by the process of
gametogony.
Pathogenesis
Transmission through
Bradyzoites/ oocysts
Disseminated to:
Skeletal muscle
Myocardium
Brain
Eyes
(Extraintestinal cycle)
Penetrate and
multiply rapidly in
GI cells
Sporozoites encyst
Transported in lymphatics
and bloodstream
Cell rupture
Transplacental transmission
If a pregnant animal becomes infected, tachyzoites can
infect the fetus via the bloodstream.
After several rounds of
asexual reproduction
(endodyogeny),
Tachyzoites are formed.
Clinical signs
In Cats
They act as definitive host for T. gondii but rarely produce clinical disease.
Clinical toxoplasmosis is most severe in transplacentally infected kittens.
•
Ocular discharge, photophobia, miotic pupils
•
Respiratory distress
•
Neurological signs: ataxia, seizures, tremors, paresis, cranial nerve defects
•
Gastrointestinal signs: vomiting, diarrhea, abdominal pain, jaundice
•
Congenital transmission:

Affected kittens may be still born or may die before weaning.

Enlarged abdomen

Encephalic kittens sleep all the time or cry continuously.
Clinical signs
In Dogs
Dogs rarely suffer from toxoplasmosis as a primary disease, and, in most cases, the disease is
linked to immunosuppression and absence of vaccination against canine distemper virus (CDV).
• Neurological signs like: seizures, ataxia, paresis
• Respiratory distress
• Gastrointestinal signs: Diarrhea, abdominal pain, jaundice
In Cattle
• Acute course- fever, dyspnea and nervous signs (including ataxia and hyperesthesia) in early
stage followed by extreme lethargy.
• Abortion
• Congenitally affected calves shows- fever, dyspnea, coughing, sneezing, nasal discharge,
clonic convulsions, grinding of teeth and tremors of head and neck
Clinical signs
In Sheep and Goat
•
Circling, incoordination, muscular rigidity and prostration
•
impaired vision and Abortion during last stage of pregnancy or still birth/weak lambs
•
Congenitally affected lambs- mentally dull, weak, incoordinated and unable to nurse.
Congenital Toxoplasmosis in Human

Fever

Jaundice

Hydrocephalus

Maculopapular and/or petechial rash

Respiratory distress

chorioretinitis (often bilateral)
Gross lesions
Lungs: interstitial pneumonia, small grey , tumor like mass in lung
Heart: Myocarditis
Intestine: granulomatous nodules
Liver: Hepatic necrosis
Brain: meningoencephalomyelitis
Eye: Chorioretinitis
Lymphnode: Lymphadenopathy (enlarged, firm and congested)
Skeletal M/s: Myositis
Aborted fetous: focal necrosis in the cotyledons, accompanied by calcification
Gross lesions
Fig: Focal placental necrosis
Fig: Closer view of an affected cotyledon
from aborted lamb
Gross lesions
Fig: Lungs and heart of a kitten congenitally
infected with Toxoplasma gondii
Pneumonia in lungs and necrosis in heart
Fig:1) Heart, Lamb. White grey necrotic areas (arrows) in the
myocardium
2) Mesenterial Lymph nodes, Lamb. Edematous and
enlarged appearance of lymph nodes
Gross lesions
Chorioretinitis in a cat with toxoplasmosis
Microscopic lesions
•
•
•
Characterized by the presence of intracellular tachyzoites, foci of necrosis, and an associated
inflammatory reaction composed mainly of mononuclear cells
Liver
 Contains large, sharply well defined areas of coagulative necrosis
Brain
 Diffuse necrotizing and non-suppurative infiltration of brain parenchyma
 Presence of Tachyzoites in brain parenchyma
•
Lungs
 Foetalization of lungs (Lining of the alveoli becomes cuboidal or columnar and rich in cells)
 Alveoli filled with large mononuclear cells and leukocytes.
•
Lymph nodes
 Extensive coagulative necrosis. Tachyzoites found near the necrotic areas
Microscopic lesions
Fig:
Photomicrograph
depicting
Fig: A – Granuloma in brain tissue. Area showing
Toxoplasma gondii
higher vascularity with acellular eosinophilic center
Severe, necrotizing, interstitial pneumonia
indicating necrosis (large arrow), surrounded by cells
with numerous intralesional protozoal tissue
with pyknotic nucleus (small arrow) and large cells with
cysts consistent with Toxoplasma gondii
epithelioid appearance (40x).
Microscopic lesions
Fig: C – Multifocal mononuclear perivascular
inflammatory
infiltrate
(large
arrow)
with
hemorrhagic foci in the myocardium (small arrow).
Invasion and segmental necrosis of muscle fibers (star)
(40x). Scale bars: A – C = 50 μm
Fig: Tissue cyst in the brain of a cat (periodic
acid – Schiff stain, × 400).
Diagnosis
•
Field diagnosis:
Signs and lesions: abortion, stillbirth, presence of white necrotic foci in placenta, etc.
•
Laboratory diagnosis:
 Animal inoculation: Intraperitoneal inoculation of suspected material into mice.
Death of mice occur with in 5-12 days. Demonstration of intracellular and free form
of Toxoplasma trophozoites in Giemsa stained smears of peritoneal exudate.
 Histopathology: Demonstration of parasite in sections of infected tissues
 Methylene blue dye test (Sabin and Feldman test)
 Serological tests: CFT, IFAT, IHA, ELISA, etc.
 Molecular Technique: PCR
Diagnosis
•
Fecal Examination
Fig: Toxoplasma oocysts (small upper left) compared with a
Capillaria egg (large lower right) in feces of a naturally infected cat
(unstained, × 400)
Diagnosis
•
Transmission Electron Micrograph
Figure: Young tissue cyst of Toxoplasma gondii
in the brain of a mouse (21 days post-inoculation).
The tissue cyst is separated from the cytoplasm of
the neuron by a parasitophorous vacuole (PV) . One
bradyzoite (arrowhead) is dividing ( × 6500).
Differential Diagnosis
•
Brucellosis
•
Listeriosis
•
Enzootic abortion
•
Salmonellosis
•
Leptospirosis
•
Campylobacter
Trypanosomiasis
Introduction
•Trypanosomosis is a group of diseases affecting mammals, domesticated and wild animals, as
well as man and birds caused by various species of Trypanosoma
•Divided into two major forms:
American Trypanosomiasis
African Trypanosomiasis
Etiology
Trypanosomes are flagellated motile protozoan parasites
Scientific classification
Class
Kinetoplastida
that live in blood and body fluids of their host and localize
in tissues, sometimes in a non flagellated form.
Order
Family
Genus
Trypanosomatida
Trypanosomatidae
Trypanosoma
Etiology
Trypanosoma species
Disease caused
Trypanosoma evansi
Surra
T. equiperdum
Dourine
T. equinum
Mal de caderas
T. congolense and T.vivax
Wasting disease in cattle
T.cruzi
Chagas disease or American Trypanosomiasis
T.gambiense
West African Sleeping sickness in man
T. rhodesiense
East African Sleeping sickness in man
T. brucei
Nagana or tse tse fly disease or African trypanosomiasis
Epidemiology
Transmission
•
Almost all trypanosomes are transmitted by arthropods (Tse tse fly), which act as biological
vectors.
(Exception : Trypanosoma equiperdum, cause of dourine, which is transmitted by coitus)
•
Mechanical transmission of trypanosomes may be done by certain biting flies (Tabanus,
Stomoxys). It is not an important route of transmission except for T. evansi which cause
Surra in horses
Pathogenesis
•
The Trypanosomes of American trypanosomiasis invade cells whereas African trypanosomiasis do not.
•
Following entry into the mammalian host, African trypanosomiasis rapidly multiply by binary fission within the blood
stream leading to parasitaemia.
•
The parasite's unique ability to undergo almost endless antigenic variations through changes in surface glycoproteins
called variable surface glycoproteins(VSGs).
•
Trypanosomes may also enter the interstitial space and multiplication occurs. Glomerulonephrits and vasculitis which may
occur in chronic trypanosmiasis can result from the continuous immune response and the formation of antigen and
antibody complexes.
•
The pathogenesis of inflammatory reactions in various tissues is also considered to be immune mediated which are
characterized by proliferation and activation of macrophages.
•
Toxic products of trypanosomes may also play a role in the pathogenesis of tissue damage which can include necrosis.
•
Adherence of organism to RBCs making it appear immunologically foreign causing erythrophagocytosis and hence
severe anemia
Pathogenesis
Probable cause of death in Trypanosomiasis
Decreased blood glucose level (Hypoglycemic shock)
Toxemia due to endotoxin (proteolytic) liberated by lysed parasites
Arrested erythrocyte production due to liberated toxin
Asphyxia or hypoxia: due to decreased blood sugar level due to which there is
increased lactic acid and reduces ability to carry oxygen by Hb
Stress factor: Loss of glucose shows stress on liver resulting in disfunctioning of liver
and toxemia
Other
 Mal de caderas
 Chagas disease
 Dourine
 Nagana
Diagnosis
1. Microscopic: Examination of blood, serous fluid and CSF often stained with Giemsa and Leishman stain
2. Biological: 1-5 ml of affected blood may be injected I/P or IV into susceptible laboratory animal.
3. Cultural: All trypanosomes can be cultured in chick embryo
4. Formal gel test: When a drop of formalin is added to 1ml of suspected serum, in positive cases, gel
formation takes place
5. Mercuric chloride test
6. Stilbamide test