Toxoplasmosis is considered one of the neglected parasitic infections of the United States, a group of five parasitic diseases that have been targeted by CDC for public health action.Q fever is a disease caused by the bacteria Coxiella burnetii. This bacteria naturally infects some animals, such as goats, sheep, and cattle. C. burnetii bacteria are found in the birth products (i.e. placenta, amniotic fluid), urine, feces, and milk of infected animals.

1. TOXOPLASMOSIS
AND Q-FEVER
PREPARED BY
DR. SWOCHHAL PRAKASH SHRESTHA
DR. SUBAS CHHETRI
DR. SUSHIL NEUPANE

2. TOXOPLASMOSIS
INTRODUCTION
 Toxoplasmosis or Crazy cat lady syndrome is a worldwide
neglected zoonotic disease which affects nearly all warm blooded
animals and human.
 It affects reproductive system, nervous system, skeletal muscles
and eyes.
 The sexual cycle occurs only in species belonging to Felidae
family.
 Individuals at risk for toxoplasmosis include fetuses, newborns,
and immunologically impaired patients.

3. DISTRIBUTION
 First time discovered in 1908 by Nicolle and Manceaux from
North African rodent (Ctenodactylus gondi).
 Incidence is more in warm, moist climates than cold, dry
climates.
 The sero-prevalence varies widely in different regions and
depends on socio-economic status, environmental factors and
meat-cooking habits.

4. ETIOLOGY
 Caused by the protozoan intracellular parasite Toxoplasma gondii,
belonging to the class Sporozoa, subclass Coccidia and order
Eucoccidia.
 There are 3 major genotypes (type I, type II, and type III) of T.
gondii. These genotypes differ in their pathogenicity and
prevalence in people.

5. SUCEPTIBLE HOST
 Involves both definitive and intermediate hosts.
 Definitive hosts are members of the family Felidae, especially the
domestic cats, along with other species like Mountain lion,
Leopard cat and Bob cat.
 Intermediate hosts include a range of warm-blooded animal like
man, birds, rodents, marsupials, and other domestic and wild
mammals.
 Toxoplasma normally divides asexually to yield a haploid form
that can infect virtually any vertebrate host but it also has a well
defined sexual cycle that occurs exclusively in cats.

6. ROUTES OF TRANSMISSION
All three stages are infectious for both intermediate and definitive
hosts which may acquire T.gondii infection by any of the following
routes:
 Horizontally by oral ingestion of infectious oocysts from the
environment.
 Horizontally by oral ingestion of tissue cysts contained in raw or
undercooked meat or viscera of intermediate hosts.
 Vertically by transplacental transmission of tachyozites.
 Tachyzoites may also be transmitted in the milk from the mother
to the offspring.

7. LIFE CYCLE
The life cycle of T. gondii is facultatively heteroxenous, with three
infectious stages:
1. Tachyzoites, also called trophozoite is the rapidly multiplying
form and can infect any cell in the body. They are found in the blood
and body fluids.
2. Bradyzoites or tissue cyst is a stage encysted in the tissue. They
are slowly multiplying form and found in the body tissues.
3. Oocyst is a cyst surrounded by a thick resistant wall and voided in
the faeces of cats.
The parasite has got affinity for epithelial, reticulo-endothelial and
blood cells.
Trophozoites and tissue cysts represent stages in asexual
reproduction while oocyst is seen in definitive hosts formed by
sexual reproduction.

10. CLINICAL FINDINGS
 Cat: fever, bilirubinemia, lymphadenitis, dyspnea, anemia, iritis,
encephalitis and intestinal obstruction. Acute disease is
characterized by anorexia, lethargy, pyrexia, dyspnea and death.
 Dog: Asymptomatic. Lesions involve lungs and central nervous
system.
 Pig: There is abortion and still births in sows and dyspnea and
wasting in young piglets.

11. CLINICAL FINDINGS
 Sheep and Goat: Abortion is the main manifestation in ewes. In
goats, acute infection is characterized by high rise of temperature,
dyspnea, diarrhea, muscular tremors, paresis of hind quarters,
erythropaenia and anaemia.
 Cattle and Buffalo: High rise of temperature and enlargement of
lymph nodes are the important clinical features.

12. CLINICAL FINDINGS
 Human: Most cases are asymptomatic. There is mild fever
leading to encephalitis. There are symptoms of rash,
lymphadenitis, chorioretinitis, and abortion in female. Child may
die or born with congenital cataract, hydrocephalus, micro-
cephalus or anencephalus condition.

13. DIAGNOSIS
 Isolation of T.gondii.
 Methylene blue dye test
 Compliment fixation test
 Indirect haemaglutination test.
 Direct agglutination test.
 Latex agglutination test
 Fluorescent antibody test.
 ELISA

14. TREATMENT
 No satisfactory treatment
 Drugs like pyremethamine and sulphonamides have been used
with success.
 Diaminodiphenyl sulfone(SDDS) @ 100mg/kg body weight for
14 days is most effective treatment.

16. CONTROL
 Direct or indirect contact with cat faeces and infected cats should
be avoided
 Thorough cooking of meat and vegetables should be ensured
 Meat should be cooked to a temperature of at least 160 C for 20
minutes.
 Drinking water should be from a clean source.
 Ensure the quality of animal origin feaces given to food animals
 Pregnant women, and persons with suppressed immune systems,
should be conscious in keeping themselves away from cat faeces.
 Control rodent populations and other potential intermediate hosts
 Do not drink unpasteurized milk.
 Wash hands and food preparation surfaces with warm soapy
water after handling raw meat.

17. REFERENCES
 Tenter, A. M., Heckeroth, A. R., & Weiss, L. M. (2000).
Toxoplasma gondii: from animals to humans. International
journal for parasitology, 30(12-13), 1217-1258.
 Negash, T., Tilahun, G., & Medhin, G. (2008). Seroprevalence of
Toxoplasma gondii in Nazareth town, Ethiopia. East Afr J Public
Health, 5(3), 211-214.
 Sonar, S. S., & Brahmbhatt, M. N. (2010). Toxoplasmosis: an
important protozoan zoonosis. Veterinary World, 3(9), 436.

18. Q-FEVER
INTRODUCTION
 Q fever is a zoonotic disease caused by the intracellular bacterium
Coxiella burnetii.
 Mostly occurs in farm animals.
 Used as an agent of bioterrorism.

19. DISTRIBUTION
 Has got global distribution but is absent in New Zealand and
Antarctica.
 Since the clinical presentation is very pleomorphic and
nonspecific, the incidence of Q fever among humans is probably
underestimated, and diagnosis particularly relies upon the
physician’s awareness of the symptoms of Q fever and the
presence of a reliable diagnostic laboratory.

20. ETIOLOGY
 Query (Q) fever, due to Coxiella burnetii, is a ubiquitous
zoonosis.
 The term “Q fever” (for query fever) was proposed in 1937 by
Edward Holbrook Derrick to describe febrile illnesses in abattoir
workers in Brisbane, Queensland, Australia in 1935.
 The name Coxiella burnetti was given on the honour of two
scientist Harold cox and Mac Fariance Burnetii.
 This belongs to the order Legionellate, family Coxiellacleae.
 It is a gram negative coccobacillary organism which used to
reside and replicate in the host macrophage and monocytes.

21. BACTERIOLOGY
 C. burnetii is an obligate intracellular, small gram-negative
bacterium (0.2 to 0.4 mm wide, 0.4 to 1 mm long).
 Although possessing a membrane similar to that of a gram-
negative bacterium, it is usually not stainable by the Gram
technique.
 The Gimenez method is usually used to stain C. burnetii in
clinical specimens or laboratory cultures.
 C.burnetii can be cultivated on cell layers from clinical or animal
samples and can persist in daughter cells without affecting the
viability of these persistently infected cells.
 Resistant to physical and chemical agents.
 Can remain viable in soil and congenial environment for many
months.

22. SUSCEPTIBLE HOSTS
 Reservoirs − Domestic animals
 Sheep, cattle, goats
 Dogs, cats − Birds − Reptiles −Wildlife

23. MODE OF TRANSMISSION
 Inhalation : soil contaminated dust, air borne dust, contaminated
wool dust, contaminated bedding. Materials are infected by
infected urine and faeces.
 Ingestion : contaminated milk, genital discharges, fetus or
placenta, bedding materials or manure
 Contact: farm workers, veterinarians, live stock dealer, dairy plant
worker, shearers, slaughter house workers
 Vector: ticks are the reservoirs and vectors for transmission.

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

25. SYMPTOMS
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%

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

27. 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

28. DIAGNOSIS
 Isolation and identification of the agent
 Serological test: IFA, ELISA and CFT.
 Antigen detection Assay: Immuno histo- chemical staining
 Nucleic acid detection P.C.R.

29. 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.

30. 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.

31. REFERENCES
 Maurin, M., & Raoult, D. F. (1999). Q fever. Clinical
microbiology reviews, 12(4), 518-553.
 Fournier, P. E., Marrie, T. J., & Raoult, D. (1998). Diagnosis of Q
fever. Journal of clinical microbiology, 36(7), 1823-1834.
 Parker, N. R., Barralet, J. H., & Bell, A. M. (2006). Q fever. The
lancet, 367(9511), 679-688.

32. THANK YOU