Parasitic zoonoses

1. SUMANABISWAS
2ND YEARB.SC(N)
MANJUSHREECOLLEGEOF NURSING
BANGALORE

2. Zoonoes also known as zoonosis, and zoonotic diseases are
infectious disease caused by bacteria, virus, and parasites
zoonos that spread between animals and humans.

3. A zoonotic parasite is a parasite that can be transmitted
between animals and people. Humans are not the primary
host, so the zoonotic parasite will act differently in humans.
Zoonotic parasites cause health problems in humans that
range from those that are minor to the very serious

4. There are three types of Parasitic Zoonoses :-
1. Taeniasis
2. Hydatid Disease
3. Leishmaniasis

6. •
A group of cestode infections which are important
zoonotic diseases. Two parasites of importance in
taeniasis are Taenia saginata and T. solium. These are
classified as "cyclo-zoonoses" because they require
more than one vertebrate host species (but no
invertebrate host) to complete their developmental
cycles.

7. Taeniasis is an infection within the intestine by adult
tapeworms belonging to the genus Taenia. It is mainly
caused by eating contaminated pork or beef

8. • This parasite is virtually global in distribution, wherever beef is
eaten. Highly endemic regions (prevalence rates exceeding 10
per cent) exist in some African countries south of the Sahara, in
Eastern Mediterranean countries and in parts of USSR. There is
a moderate prevalence in Europe, in most of the Indian
subcontinent, Southern Asia, and in Japan.
• T. solium infection is endemic in many countries of Latin
America, Africa and Asia as well as in some parts of Europe and
the USSR (2). It is endemic in India, and has been widely
reported

9.  Agent
(T. Solium & T. Saginata)
 Host
• Cow
• Pig
 Environment
• Undercooked meat
• Contaminated Food
• Reinfection

10. •Taenia saginata (beef tapeworm)
•Taenia solium (pork tapeworm)

11. T. solium
T. saginata

12. • T. saginata and T. solium pass their life cycles in two hosts.
In man, the adult parasites live in the small intestine.
• The adult T. saginata measures 5 to 12 metres in length,
and may be up to 24 metres; T. solium measures 2 to 6
metres.
• The larval stage of T. saginata (C. bouis) mainly occurs in
cattle. The pig is the main host for the larval stage of T.
solium (C. cellulosae) but man may also be infected.
• The adult stages of T. saginata and T. solium may persist
for several years in infected humans

13. Pork (Pig)
Beef (Cow)

14. • Undercooked Meat
• Contaminated food
• Reinfection

15. These infections are acquired :
1. Through the ingestion of infective cysticerci in undercooked
beef (T. saginata) or pork (T. solium).
2. Through ingestion of food, water or vegetables contaminated
with eggs.
3. Reinfection by the transport of eggs from the bowel to the
stomach by retroperistalsis.

16. For the adult tapeworm, from 8 to 14 weeks.

18. • Nausea
• Gastro-Intestinal Upset
• Hunger Pain
• Diarrohea
• Constipation
• Chronic Indigestion
• Vomitting
• Blood in Stool

19. 1. Stool Examination
2. Immunological Test (Detect the presence of cysticerci)
3. MRI
4. CT Scan(To detect cysticerci in various organ)
5. Blood Test

20. The methods usually employed for control are :
• Early detection
• Treatment of infected persons.
• Meat inspection.
• Health education.
• Adequate sewage treatment and disposal.
• By the proper housing and feeding of pigs.

21. • Thorough cooking of beef and pork is the most effective method
to prevent food-borne infections.
• Improvement of living conditions, especially safe treatment of
sewage used for farming, should be aimed at.
• Education of the public to prevent pollution of soil, water and food
with human faeces, and washing of hands before eating and after
defecation, are important health educational messages.

22. • Praziquantel is given in a single dose of 10 mg/kg. body wt. It
achieves cure rates of about 99 per cent.
• Niclosamide 2grams empty stomach.
Note :- The tablets must be chewed thoroughly and swallowed
with water. Eating may be resumed after 2 hours.
• For the treatment of T. solium, give moderate purgative 2-3
hours after the drug to rapidly eliminate segments and eggs
from the bowels.

24. Hydatid disease is a zoonoses a group of cestode
infections which are important zoonotic diseases of
man. The disease in man is caused by the metacystode
stage (infective larva) of the canine intestinal tapeworm
Echinococcus; the adult worms are found in dogs and
other carnivores.

25. Hydatid disease (also known as hydatidosis or
echinococcosis) is a potentially serious, sometimes fatal,
condition caused by cysts containing the larval stages of
the Echinococcus granulosus (E. granulosus) tapeworm
(Dog Tapeworm).

26. • In recent years, hydatidosis has been recognized as a
public health problem of nearly global dimensions.
• It is found in all sheep-raising countries, e.g., Australia,
New Zealand, Tasmania, Middle East countries, Turkey,
Greece, USSR, Cyprus, Latin America and the Far East etc.
• In India where the highest prevalence is reported in
Andhra Pradesh and Tamil Nadu than in other parts of the
country.
• The prevalence of the disease is reported to be high in
food animals in India.

27.  Agent
(E.granulosus, E.multilocularis, E. Oligarathus, E. Vogeli)
 Host
• Dogs
• Catss
• Shepheards and their
families
• Shoe makers
 Environment
• Low temperature
• Heavy rainfall
• High humidity

28. • (a) E. Granulosus : It is of worldwide distribution, is for the
most part, maintained in the domestic transmission cycle
involving the dog as final host. In man the infective larva
causes hydatidosis.
• (b) E. multilocularis : It is restricted to the northern
hemisphere. It has been detected increasingly in various
countries (e.g. Iran, Turkey}. In man, the metacystode causes
the "alveolar" type of the disease.
• (c) E. oligarthus: a species occurring in Central and South
America is suspected to cause disease in man.
• (d) E. Vogeli : a species occurring in Central and South

29. E.granulosus
E.multilocularis
E.vogeli

30. • The main hosts are Sheep and Dogs.
• Human infection is acquired usually in childhood through
contact with infected dogs.
• Hydatid disease is an occupational disease of certain groups,
e.g., shepherds and their families in endemic areas and shoe-
makers.

31. • Climatic conditions including low mean annual air temperature.
• High mean annual rainfall and high humidity of the soil.

32. • Human infection occurs by ingestion of the eggs of
Echinococcus inadvertently with food.
• Unwashed vegetables or water contaminated with faeces from
infected dogs.
• Infection can also take place while handling or playing with
infected dogs, e.g., hand to mouth transfer of eggs.
• Inhalation of dust contaminated with infected eggs.
• Carnivores get infected by eating viscera containing hydatid
cysts.

33. • Incubation period is variable from month to years, depending
upon the numbers and location of cysts and how rapidly they
grow

35. • Tough hemoptysis
• Chest paIn
• Dyspnea
• Abdominal pain
• Dull ache
• Fever
• Headache
• Nausea
• Vomitting
• Blood in stool
• Diarrohea

36. Laboratorytestsinclude:-
1. Clinical
2. X-Ray
3. Serological

37. 1. There is no specific treatment excepting surgical removal of
cysts which is not without considerable risk in as much as the
accidental penetration of one of the cysts can lead to
anaphylactic shock which may prove fatal.
2. Mebendazole (Vermox) has been tried and found very
effective in mice. It may well become the drug of choice.

38. 1. Preventing dogs from gaining access to raw offal at slaughter
houses and on farms.
2. Control of slaughter houses, proper meat inspection and
destruction of infected viscera.
3. This involves eliminaion of stray dogs, drastic reduction of dog
population, an effective dog-registration system; surveillance of
dogs based on periodic stool examinations after administration of a
teanifuge such as arecoline hydrobromide, followed by the isolation
and treatment of infected animals with praziquantel. A single oral
dose of 5 mg/kg of body weight will remove all adult worms from
the dog.
4. Health education of the public particularly butchers, dog owners,
animal breeders and shepherds is the basis of effective prevention.

39. 3.LEISHMANIASIS

40. Leishmaniasis are a group of protozoa! diseases caused by
parasites of the genus Leishmania, and transmitted to man by
the bite of female phlebotomine sandfly. They are responsible
for various syndromes in humans kala-azar or visceral
leishmaniasis (VL), cutaneous leishmaniasis (CL), muco-
cutaneous leishmaniasis (MCL), anthroponotic cutaneous
leishmaniasis (ACL), zoonotic cutaneous leishmaniasis (ZCL),
post-kala-azar dermal leishmaniasis (PKDL), etc.

41. A tropical and subtropical disease caused by
leishmania and transmitted by the bite of sandflies. It
affects either the skin or the internal organs.

42. WORLD :-
• Leishmaniasis is endemic in many countries in tropical and
subtropical regions, including Africa, Central and South
Americas, Asia and the Me.diterranean region.
• More than 90 per cent of all cases of cutaneous leishmaniasis
occur in Afghanistan, Algeria, Brazil, Colombia, the Islamic
Republic of Iran, Peru, Saudi Arabia and the Syrian Arab
Republic.
• About 200,000-400,000 cases of kala-azar (visceral
leishmaniasis) are reported annually worldwide. Six countries,
namely India, Bangladesh, Brazil, Nepal, Ethiopia, South Sudan

43. INDIA :-
• Kala-azar is endemic in 52 districts in Bihar (31), Jharkhand
(4), West Bengal (11) and Uttar Pradesh (4). About 130 million
population is at risk of the disease. The present situation is
shown in Table 1.
TABLE 1

44.  Agent
(Leishmania donovani, L. Tropica, L. braZiliensis)
Host
• Age
• Sex
• Population movement
• Socio economic status
• Malnutrition
• Occupation
• Immunity
 Environment
• Altitude
• Season
• Climate change
• Rural area
• Vectors
• Development projects

45. The leishmania are intracellular parasites. They infect and divide
within macrophages.
• Leishmania donovani is the causative agent of kala-azar.
• L. tropica is the causative agent of cutaneous leishmaniasis.
• L. braziliensis is the causative agent of muco-cutaneous
leishmaniasis.
A. Reservoir Of Infection:-
• There is a variety of animal reservoirs, e.g., dogs, jackals,
foxes, rodents and other mammals. Indian kala-azar is
considered to be a non-zoonotic infection with man as the sole

46. (a)AGE:- Kala-azar can occur in all age groups including infants below
the age of one year. In India, the peak age is 5 to 9 years.
(b)SEX:- Males are affected twice as often as females.
(c)POPULATION MOVEMENT:- Movement of population (migrants,
labourers, tourists) between endemic and non-endemic areas can
result in the spread of infection.
(d)SOCIO-ECONOMIC STATUS:- Kala-azar usually strikes the poorest
of the poor. Poverty increases the risk for kala-azar. Poor housing
and domestic sanitary conditions (e.g. LEISHMANIAS!S lack of waste
management, open sewerage) may increase sandfly breeding and
resting sites, as well as their access to humans. Sandflies are
attracted to crowded housing as these provide a good source of
blood-meal.

47. (e) MALNUTRITION :- Diets lacking protein-energy; iron,
vitamin A and zinc increases the risk that an infection will
progress to kala-azar.
(f) OCCUPATION :- The disease strongly associates with
occupation. People who work in various farming practices,
forestry, mining and fishing have a great risk of being bitten by
sandflies.
(g) IMMUNITY :- Recovery from kala-azar and oriental sore
gives a lasting immunity. During the active phase of kala-azar,
there is impairment of cell mediated immunity, this is reflected
in the negative skin reaction to leishmanin test.

48. (a)ALTITUDE : Kala-azar is mostly confined to the plains; it does
not occur in altitudes over 2000 feet.
(b)SEASON : In the past epidemics, two peaks, one in November
and another in March-April were reported. Generally there is
high prevalence during and after rains.
(c)CLIMATE CHANGES : Kala-azar is climate sensitive, and is
strongly affected by changes in rainfall, temperature and
humidity. Global warming and land degradation together
affect the epidemiology of kala-azar in many ways.

49. (d) RURAL AREAS : The disease is generally confined to rural
areas, where conditions for the breeding of sandflies readily
exist compared to urban areas.
(e) VECTORS : In India, P. argentipes is a proven vector of kala-
azar. Cutaneous leishmaniasis is transmitted by P. papatasi and
P. sergenti. Sandflies breed in cracks and crevices in the soil and
buildings, tree holes, caves etc. Overcrowding, ill-ventilation and
accumulation of organic matter in the environment facilitate
transmission.
(f) DEVELOPMENT PROJECTS: Ironically many development
projects are exposing more people to leishmaniasis. Forest
clearing, and cultivation projects, large water resource schemes,
and colonization and resettlement programmes.

50. • Kala-azar is transmitted from person to person by the bite of
the female phlebotomine sandfly, P. Argentipes.
• Transmission may also take place by contamination of the bite
wound or by contact when the insect is crushed during the act
of feeding.
• Transmission of kala-azar has also been recorded ·by blood
transfusion and is also possible by contaminated syringes and
needles

51. The incubation period in man is quite variable,
generally 1 to 4 months; range is 10 days to 2
years.

52. • High fever
• Weight loss
• Spleenomegaly
• Hepatomegaly
• Anemia
• Malaise
• Hyper pigmentation of forehead, abdomen and hand

53. • Occasional bleeding
• Weakness
• Lymphadenopathy
• Ulcers in the mouth
• Skin ulcer
• Reduced RBC Production

54. 1.Parasitological diagnosis:- The demonstration of the parasite
LD bodies in the aspirates of the spleen, liver, bone marrow,
lymph nodes or in the skin (in the case of CL) is the only way to
confirm VL or CL conclusively. The parasite must be isolated in
culture to confirm the identity of the parasite.
2. Aldehyde test:- The aldehyde test of Napier is a simple test
widely used in India for the diagnosis of kala-azar. 1 to 2 ml of
serum from a case of kala-azar is taken and a drop or two of 40
per cent formalin is added. A positive test is indicated by
jellification to milk-white opacity like the white of a hard-boiled
egg so that in ordinary light newsprint is invisible through it. If it
occurs within 2 to 20 minutes, it is said to be strongly positive.

55. 3 Serological tests :- Of the numerous serological tests available,
Direct Aggutination test (DAT), rk39 dipstick test, ELISA and the
indirect fluorescent antibody test (IFAT) are considered most
suitable. The ELISA test has a wide potential both for diagnosis
as well as for epidemiological field surveys.
• The rk39 -rapid diagnostic test is based on the recombinant k
39 protein. The test is simple to perform and yields result
within five minutes.
4. Leishmanin (Montenegro) test:- An intradermal injection of
0.1 ml of 10^6 per ml washed promastigotes of leishmania,
suspended in 0.5 per cent phenol saline or merthiolate on the
flexor surface of the forearm is given and examined after 48 to
72 hours. Induration is measured and recorded. An induration of

56. 5. Haematological findings :- These include progressive
leucopenia, anaemia and reversed albumin-globulin ratio, with
greatly increased IgG. The WBC:RBC ratio is 1:1500 or even
1:2000 (normal 1:750). ESR is increased.

57. The drug policy under Kala-azar elimination programme as per
recommendation of Expert Committee (2000) is as follows:-
A.
1. First line drugs-short-term :
a. In areas with sodium stibogluconate (SSG) sensitivity more than
90 per cent. -SSG 20 mg/kg body wt/day (maximum 850 mg/
day) intramuscular or intravenous for 20 days, if partial response
to 20 days treatment then continue for 30 days.
b. b. In areas with SSG sensitivity less than 90 per cent
Amphotericin B lmg/kg body wt intravenous infusion daily or
alternate day for 15-20 infusions, dose can be increased in
patients with incomplete response with 30 injections.

58. 2. First line drugs-long-term :
a. In areas with high level of SSG resistance(> 20%)
– Miltefosine 100 mg daily in two divided doses for 4
weeks. (2.5 mg/kg body wt/day in two divided doses).
a. In areas with SSG sensitivity > 80 per cent
–SSG IM or IV 20 mg/kg/day for 30 days. Miltefosine
100 mg daily for 4 weeks (after phase III studies completed with
proven safety and efficacy).

59. B.
Second line drugs
1. SSG failures
–Amphotericin B lmg/kg body wt, IV infusion daily or
alternate day for 15-20 infusions. Dose can be increased in patients
with incomplete response with 30 injections.
2. SSG and Miltefosine failure
–Liposomal Amphotericin B (when final results are
available with proven efficacy and safety) Treatment of PKDL : SSG in
usual dosage for kala-azar could be given for 120 days. -Repeated 3-
4 courses of Amphotericin B can be given in patients failing SSG
treatment.

60. • A new drug namely "Liposomal Amphotericin B" in dose of 10
mg, administered intravenously as a single dose therapy has
been introduced in the Kala-azar therapy. It will help. reduce
human reservior as it cures the patient with a single shot.

61. 1. Control of reservoir :-
Since man is the only reservoir of kala-azar in India, active and
passive case detection and treatment of those found to be
infected may be sufficient to abolish the human reservoir and
control the disease. House-to-house visits and mass surveys
may be undertaken in endemic areas for early detection of cases.

62. 2. Sandfly control :-
• The application of residual insecticides has proved effective in
the control of sandflies. DDT is the first choice since the vector
of kala-azar, P. argentipes is susceptible to DDT.
• Insecticide spraying should be undertaken in human dwellings,
animal shelters and all other resting places upto a height of 6
feet (2 metres) from floor level.
• DDT (two rounds per year) at the rate of 1-2 g per sq. metre is
considered sufficient to control transmission.
• Any sign of resistance in vector should lead to an immediate
change in insecticide. BHC (benzene hexachloride) be kept as a
second line of defence.

63. • Spraying should be repeated at regular intervals to keep down
the density of sandflies. For long-lasting results, insecticidal
spraying should be combined with sanitation measures, viz
elimination of breeding places (e.g., cracks in mud or stone
walls, rodent burrows, removal of firewood, bricks or rubbish
around houses), location of cattle sheds and poultry at a fair
distance from human dwellings, and improvement of housing
and general sanitation.

64. 3. Personal prophylaxis :-
• The risk of infection can be reduced through health education.
• By the use of individual protective measures such as avoiding
sleeping on floor, using fine-mesh nets around the bed. Insect
repellents (in the form of lotions, creams, or sticks).
• Keeping the environment clean.