Toxoplasmosis is caused by the protozoan Toxoplasma gondii. Cats are critical to its life cycle by shedding oocysts in their feces. Humans can be infected by ingesting undercooked meat containing cysts or through contact with contaminated cat feces or soil. While most infections are asymptomatic, it can cause severe issues in fetuses if a woman is infected during pregnancy. Treatment involves pyrimethamine, sulfonamides and folinic acid. Prevention focuses on good hygiene and avoiding contact with cat feces.

1. Toxoplasmosis; A protozoan
zoonosis
Subash Chhetri
B.V.Sc & A.H, 9th Sem
Class Roll no: 38

2. Introduction
• Toxoplasmosis is a zoonotic disease
• Caused by Coccidian protozoan Toxoplasma gondii
• Infects a wide range of animals, birds but does not appear to cause
disease in them.
• A disease of the blood and lymphatic system.
• Cats are a critical part of the life cycle.
• It is usually acquired by eating undercooked meats but can also be
acquired by contact with cat feces.
• Primary problem is a congenital infection of fetus, resulting in either a
stillbirth or a child with severe brain damage

3. Life Cycle
• The three stages of T. gondii
• (i) Tachyzoites (trophozoites): rapidly proliferate and destroy infected
cells during acute infection.
• (ii) Bradyzoites: slowly multiply in tissue cysts.
• (iii) Sporozoites in oocysts. Cats become infected with T. gondii by
carnivorism or by ingestion of oocysts

4. Life Cycle

5. Epidemiology and Transmission
• Toxoplasmosis is one of the most common infections of humans
throughout the world(30 – 50% of global population exposed or chronically
infected)
• Infection is more common in warm climates and at lower altitudes
• Human infection may be acquired in several ways:
• ◦ Ingestion of undercooked infected meat containing T. gondii cysts
• ◦ Ingestion of the oocyst from fecally contaminated hands, food, or water.
• ◦ Organ transplantation or blood transfusion
• ◦ Transplacental transmission
• ◦ Accidental inoculation of tachyzoites

6. Zoonosis
• The two major routes of transmission to humans are oral and
congenital
• In human, The tachyzoites are pressured by the host’s immune
response to transform into bradyzoites and form tissue cysts; these
cysts may remain throughout the life of the host
• Clinical disease may appear if the host becomes immuno
suppressed and the cysts rupture, releasing the parasites.

7. Infection in animals
• Most infected cats are asymptomatic, but generalized acute, subacute and
chronic (months to years) infections have been reported, particularly in
young or immunocompromised animals. Respiratory, hepatic and
pancreatic involvements occur. CNS signs, particularly common in older
cats, vary with the site of the lesion. Ocular signs are common.
• Most infected cats are asymptomatic, but generalized acute, subacute and
chronic (months to years) infections have been reported, particularly in
young or immunocompromised animals. Respiratory, hepatic and
pancreatic involvements occur. CNS signs, particularly common in older
cats, vary with the site of the lesion. Ocular signs are common.
•

8. Contd.
• In other animal species, infections are generally asymptomatic,
although outbreaks with generalized infections, abortions, stillbirths
and neonatal mortality are occasionally reported in swine. Fever,
encephalitis, ataxia and retinal degeneration have been reported in
horses.
• Transmissible only within felidae.

9. Infection in human
• 1- Acquired in the immunocompetent patient
• Generally an asymptomatic infection.
• 10 to 20% of patients with acute infection may develop cervical
Lymphadenopathy and/or a flu-like illness.
• The clinical course is benign and self limited
• Symptoms usually resolve within weeks to months.

10. Contd.
• 2 - Acquired or reactivated in the immunodeficient patient
• Immunodeficient patients often have central nervous system(CNS)
disease but may have myocarditis or pneumonitis.
• In patients with AIDS, Toxoplasmic encephalitis is the most common
cause of intracerebral mass lesions
• Toxoplasmosis in immunosuppressive drugs using patients due to
either newly acquired or reactivated latent

11. Contd.
• Congenital
• Congenital toxoplasmosis results from an acute primary infection
acquired by the mother during pregnancy.
• The incidence and severity vary with the trimester during which
infection was acquired.
• Treatment of the mother may reduce the severity of symptoms in
the infant, So an accurate diagnosis is extremely important
• Many infants with subclinical infection at birth will subsequently
develop signs or symptoms of congenital toxoplasmosis
• Treatment may help prevent subsequent symptoms.

12. Contd.
• Ocular
• Ocular toxoplasmosis, an important cause of Chorioretinitis in the
United States, may be the result of congenital or acquired infection
• Congenitally infected patients are often asymptomatic until the
second or third decade of life
• Lesions develop in the eye presumably due to cyst rupture and
subsequent release of tachyzoites and bradyzoites.
• Chorioretinitis is characteristically bilateral in congenital infection but
is often unilateral in individuals with acute acquired T. gondii
infection.

13. Treatment
• The most common drug combination used to treat congenital
toxoplasmosis consists of Pyrimethamine and a Sulfonamide plus Folinic
acid in the form of leucovorin calcium to protect the bone marrow from
the toxic effects of pyrimethamine.
• Pyrimethamine inhibits dihydrofolate reductase, which is important in the
synthesis of folic acid and produces a reversible depression of the bone
marrow.
• Sulfonamides inhibit synthesis of dihydrofolic acid, also important in the
synthesis of folic acid.
• After the 18th week, pyrimethamine and sulfadiazine may be given if fetal
infection is confirmed by amniocentesis or cordocentesis.
• Spiramycin is recommended for pregnant women with acute
toxoplasmosis when fetal

14. Prevention and Control
• Avoidance of human contact with Cat feces is highly important
measure.
• Changing of Cat litter and safe disposal can prevent transmission
• Pregnant women should avoid contact with kittens
• Avoid eating raw or undercooked meat.

15. References
• Dubey, J. P., & Beattie, C. P. (1988). Toxoplasmosis of animals and
man. CRC Press, Inc..
• Weiss, L. M., & Dubey, J. P. (2009). Toxoplasmosis: A history of clinical
observations. International journal for parasitology, 39(8), 895-901.
• Teutsch, S. M., Juranek, D. D., Sulzer, A., Dubey, J. P., & Sikes, R. K.
(1979). Epidemic toxoplasmosis associated with infected cats. New
England Journal of Medicine, 300(13), 695-699.

17. Q Fever : A bacterial zoonotic
disease
Subash Chhetri
B.V.Sc & A.H, 9th Sem
Class Roll no: 38

18. Introduction
• Coxiella burnetti is the causative agent of ‘Q-fever’
• Obligate intracellular, gram negative bacterium
• Distributed globally
• Found in many species of animals

19. Morphology
• obligate intracellular pathogen .
• gram negative .
• Pleomorphic .
• size : rods:- 0.2 – 0.4 x 0.4 – 1.0 mc spheres :- 0.3 – 0.4 mc filterable
• better stained with GIMINEZ and other Rickettsial stains .

20. Epidemiology
• Worldwide − Except New Zealand
• Reservoirs − Domestic animals
• Sheep, cattle, goats
• Dogs, cats − Birds − Reptiles −Wildlife

21. Transmission
• Bacteria excreted in feces, urine and milk of infected animal.
• During birthing the organisms are shed in high numbers in amniotic fluids
and the placenta
• 109bacteria per gram of placenta.
• Aerosol:-Most common −
• Parturient fluids - 109 bacteria per gram of placenta −
• Urine, feces, milk − Wind-borne:-Contaminated dust, manure, birthing
products
• Direct contact
• Fomites • Ingestion • Arthropods (ticks)

22. Human-Human Transmission
• Person-to-person (rare) −
• Trans placental (congenital) −
• Blood transfusions −
• Bone marrow transplants −
• Intradermal inoculation −
• Possibly sexually transmitted

24. Public Health Significance
• Acute Q fever
• Self-limiting, flu-like disease
• Fever, nausea, headaches, vomiting, chest/abdominal pain
• Pneumonia & granulomatous hepatitis
• Other signs (< 1%) ;Myocarditis, pericarditis, meningo encephalitis
• Death: 1-2%

25. Chronic Symptoms (>6 months)
• Endocarditis & meningo encephalitis
• Pre-existing disease
• 1-5% of those infected
• Prior heart disease,
• pregnant women,
• immune compromised
• Other ; Osteomyelitis, Granulomatous hepatitis, Cirrhosis

26. Pathogenesis
• Entry via inhalation
• Alveolar macrophages encounter bacteria
• C. brunetii phagocytized
• Replication within phagocytes
• Low pH needed for metabolism
• No cellular damage unless lyses occurs
• Can invade deeper tissue and cause complications

27. Animal Disease
• Sheep, cattle, goats −
• Usually asymptomatic −
• Reproductive failure; Abortions, still births, Retained placenta,
Infertility, Rarely fatal to animals
• Weak newborns, Low birth weights
• Mastitis in dairy cattle −
• Carrier state − Has been found in other animal species − Dogs, cats,
horses, rabbits, birds

28. Treatment
• Once infected, humans can have life-long immunity
• Acute Q fever treated with: Doxycycline (100 – 200 mg/day)
• Chloramphenicol (Adult : 50 – 100 mg/kg/day Child : 25 –
50mg/kg/day)
• Erythromycin (Adult : 1-2 g/day up to 4gm/day Child : 30 -50 mg/day
up to 1g/day)
• Timethoprim/sulfamethoxazole (160/800 mg)
• Fluoroquinolones:- Ciprofloxacin, Gemifloxacin, Levofloxacin,
Moxifloxacin Norfloxacin, Ofloxacin

29. Prevention and Control
• Pasteurization
• Vaccination :- prepared from formalin killed whole cells attenuated
strains trichloro acetic acid extracts − Human and animal
• Eradication not practical − Too many reservoirs − Constant exposure −
Stability of agent in environment.
• Education − Sources of infection
• Good husbandry − Disposal of birth products (incinerate), Lamb
indoors in separate facilities − Disinfection 0.05%, chlorine 1:100,
Lysol
• Isolate new animals

30. References
• Maurin, M., & Raoult, D. F. (1999). Q fever. Clinical microbiology
reviews, 12(4), 518-553.
• Parker, N. R., Barralet, J. H., & Bell, A. M. (2006). Q fever. The
lancet, 367(9511), 679-688.
• Jekel, J. F., Katz, D. L., Elmore, J. G., & Wild, D. (2007). Epidemiology,
biostatistics and preventive medicine. Elsevier Health Sciences.

31. THANKYOU !!!