the presentation is about the protozoan diseases transmitted form animals to humas and wise versa

1. ZOONOSES BY
PROTOZOANS
Dr. NEETHU K P
Dept. of Vet. Public Health
College of Veterinary and Animal Sciences, Mannuthy, Kerala

2. INTESTINAL PROTOZOAL
INFECTION
SYSTEMIC PROTOZOAL
INFECTION
• Amoebiasis
• Giardiasis
• Cryptosporidiosis
• Balantidiasis
• Cyclosporidiosis
• Microsporidiosis
 Toxoplasmosis
 Leishmaniasis
 African trypanosomiasis
(sleeping sickness)
 American trypanosomiasis
(Chagas’ disease)
 Malaria
 Babesiosis

3. TOXOPLASMOSIS
 Toxoplasma gondii
 Subphylum Apicomplexa
 Family Eimeriidae

4.  Obligate intracellular parasite
 Definitive host – cats
 Intermediate hosts – sheep, goats, pigs, humans
 All warm-blooded animals, including mammals and birds
 Second commonest opportunistic infection inAIDS patients, with
as high as 75 % mortality

5. Distribution
Dark red- >60% Yellow- 20-40% Green- <1%
Red – 40-60% Blue- 10-20% White- Absence of data

6. In INDIA…
 The prevalence of toxoplasmosis in India was as high as 77%
in women of reproductive age
 IgG and IgM antibodies were found in 24.3% and 2% of the
samples, respectively
 A higher prevalence ofT. gondii infection has been recorded
in women belonging to low socio-economic groups
(Dumne et.al,2007)

7.  Higher seroprevalence was observed in pigs (14.0%), sheep
(7.9%), goats (8.8%) and camels (7.5%)
 The prevalence ofT. gondii in cats (2.5%) is low when
compared with that inWestern countries
 The incubation period is uncertain but probably ranges from
5–23 days in humans

8. PATHOPHYSIOLOGY
 There are three infective stages of T. gondii:
 Rapidly dividing invasive tachyzoite
 Slowly dividing bradyzoite in tissue cysts
 Environmental stage, the sporozoite, protected inside an
oocyst

11. MODES OF TRANSMISSION

12. Contd….
 Toxoplasmosis can be transmitted transplacentally if the mother
becomes infected during pregnancy or if immunosuppression
reactivates a prior infection.
 Transmission ofToxoplasma to a fetus is extraordinarily rare in
immunocompetent mothers who have had toxoplasmosis earlier
in life.
 Past infection confers resistance to reinfection.

13. DISEASE IN MAN
 Acute toxoplasmosis
 CNS toxoplasmosis
 Congenital toxoplasmosis
 Ocular toxoplasmosis
 Disseminated or non-CNS disease in immunocompromised
patients

14. ACUTE TOXOPLASMOSIS
 Asymptomatic
 10 to 20% of patients develop bilateral, nontender cervical
or axillary lymphadenopathy.
 Mild flu-like syndrome of fever, malaise, myalgia,
hepatosplenomegaly
 Self-limited.

15. CNS TOXOPLASMOSIS
 Most patients withAIDS or other immunocompromised
patients with encephalitis
 Headache, altered mental status, seizures, coma, fever
 Focal neurologic deficits, such as motor or sensory loss,
cranial nerve palsies, visual abnormalities, focal seizures.

16. CONGENITAL TOXOPLASMOSIS:
 Spontaneous abortion, stillbirth, birth defects
 The percentage of surviving fetuses born with toxoplasmosis
depends on when maternal infection is acquired
 15% during the 1st trimester
 30% during the 2nd
 60% during the 3rd.
 Most infants born to mothers infected during the 3rd trimester
appear healthy at birth but are at high risk of seizures,
intellectual disability, retinochoroiditis

17.  Disease in neonates - severe, particularly if acquired early in
pregnancy; - jaundice, rash, hepatosplenomegaly
 Characteristic tetrad of abnormalities: bilateral
retinochoroiditis, cerebral calcifications, hydrocephalus or
microcephaly and psychomotor retardation.
 Prognosis is poor.

18. OCULAR TOXOPLASMOSIS
 This type usually results from congenital infection that is
reactivated, often during the teens and 20s, but rarely, it
occurs with acquired infections.
 Focal necrotizing retinitis
 Secondary granulomatous inflammation of the choroid
 Ocular pain, blurred vision, sometimes blindness.

19. DISSEMINATED INFECTION AND NON-
CNS INVOLVEMENT:
 Less common
 Primarily in severely immunocompromised patients.
 Pneumonitis, myocarditis, polymyositis, diffuse
maculopapular rash, high fevers, chills, and prostration.
 Untreated disseminated infections are usually fatal.

20. DISEASE IN CATS
 Most postnatally acquired infections in cats are
ASYMPTOMATIC.
 Prepatent period variable - 3 days to several weeks.
 Shedding occurs for 1-2 weeks

21. DIAGNOSIS:
 Sabin- Feldman DyeTest: most sensitive test, but rarely used.
 IFA
 Latex agglutination test
 ELISA.
 MRI
 Brain biopsy
 Tachyzoites in blood or body fluids confirms active infection.

22. SABIN-FELDMAN DYE TEST
 Live tachyzoites stain blue with alkaline methylene blue dye.
 Live tachyzoites are mixed with different dilutions of the
patient's serum
 The mixtures are then incubated for an hour, stained with dye,
and examined with a microscope.
 If antibodies toT gondii are present in the patient's serum, they
will damage the organisms.
 The damaged organisms will not take up the dye and appear as
pale "ghosts" compared to undamaged organisms.
 Test is very sensitive and specific and remains the reference
method.

23. TREATMENT IN MAN:
 The treatment of choice is pyrimethamine plus either
trisulfapyrimidines or sulfadiazine.
 Folinic acid is given to avoid the hematologic effects of
pyrimethamine-induced folate deficiency.

24. PREVENTION/CONTROL:
 Freezing of meat to -20ºC (-4ºF) for 2 days or heating to
60ºC (140ºF) kills cysts.
 Children's play areas should be protected from cat and dog
feces.
 Daily cleaning of cat litter pans (since oocysts not infective
for 2 to 3 days)
 Wear gloves
 Wash hands before eating
 Should only be fed dry, canned, or cooked meats
 Pregnant women shouldn’t handle cats

25. AFRICAN TRYPANOSOMIASIS
 African Sleeping Sickness
 GambianTrypanosomiasis
 RhodesianTrypanosomiasis
 Cattle -Nagana.

26.  Trypanosoma brucei gambiense and T brucei rhodesiense
 T.b.brucei - rarely infects humans-T. brucei are lysed by a factor
in human serum, whereas T. rhodesiense and T. gambiense are
not.
 Vector: tsetse fly (Glossina palpalis,G.tachinoides,or G.fuscipes).

27.  Trypanosoma brucei gambiense is found in 24 countries in west
and central Africa.
 Accounts for more than 98% of reported cases of sleeping
sickness
 Causes a chronic infection.
 Trypanosoma brucei rhodesiense - 13 countries eastern and
southernAfrica.
 2% of reported cases
 Causes an acute infection
 In 2009, the number of cases reported was 9878
 2012 there were 7216 cases recorded. (who,2013)

28. RESERVOIRS
 Many wild and domestic animals harbour infection
 In Rhodesian trypanosomiasis - domestic cattle and pigs
 In Gambian trypanosomiasis, humans are the main reservoir
 However the precise epidemiological role of the animal
reservoir in the gambiense form of the disease is not yet well
known.

29. DISTRIBUTION

30. TRANSMISSION:
 Transmission is by the tsetse fly bite.
 Mother-to-child infection: the trypanosome can cross the
placenta and infect the fetus.
 Mechanical transmission through other blood sucking insects
is possible.
 Accidental infections have occurred in laboratories due to
pricks from contaminated needles.

32. DISEASE IN ANIMALS:
 Occasionally mild disease occurs in domestic animals

33. DISEASE IN HUMANS:
1. The trypanosomal chancre:
 Seen at site of the tsetse bite
 Appears about 48 hours after and lasts 2-4 weeks.
 Local pruritic, painful inflammatory reaction with regional
lymphadenopathy

34. 2. The hemolymphatic stage:
 Usually absent or unnoticed in T.b.gambiense infections.
 Irregular fevers, headaches, joint pains,
malaise, pruritus, papular skin rash, edemas.
 Myocarditis
 Trypanosomes enter the lymphatics - lymphadenopathy - T.
gambiense is the enlarged cervical lymph nodes, called
Winterbottom’s sign

35. 3.The meningoencephalitic stage:
 Insomnia
 Motor and sensory disorders
 Abnormal reflexes
 Somnolence to coma.

36. DIAGNOSIS:
 Definitive diagnosis requires identifying the organism in the
bite lesion, blood, lymph node aspirate, or CSF.
 Serologic tests become positive after 12 days.
TREATMENT:
 Hemolymphatic stage: Suramin, eflornithine or pentamidine.
 Late disease: melarsoprol or eflornithine or tryparsamide
plus suramin.

37. PREVENTION/CONTROL:
 Wear long sleeves and trousers in endemic areas
 Use mosquito nets while sleeping.
 Repellents do not work on tsetse flies.
 Pentamidine is used as a chemoprophylaxis against the
Gambian type.

38. A new form of human Trypanosomiasis in
India
 First human case of T evansi infection in humans was
reproted in the district of Chandrapur in Maharashtra
 He had presented episodes of fever associated with
sensory disorders
 The patient continued to present peaks of fever at 7–10-
day intervals, with systematically high blood parasite
levels

39. AMERICAN TRYPANOSOMIASIS
 Chagas's Disease
 Chagas-Mazza Disease
 South AmericanTrypanosomiasis
 Trypanosoma cruzi
 Reduvid bugs

40. RESERVOIR AND INCIDENCE
 Dogs, cats, and guinea pigs are the main reservoirs for human
infection.
 T.cruzi occurs only in theAmericas- Southern South America
to northern Mexico,Texas, and the south western U.S.
 An estimated 12 million people are infected, mostly in rural
areas, resulting in about 60,000 deaths yearly.

41. TRANSMISSION:
 Humans are infected when the insect's feces become rubbed
into the wound caused by the bite of an infected
bloodsucking insect (triatomid) or when the conjunctiva,
mucous membranes or abrasions become contaminated.
 Blood transfusions from infected persons
 Congenital infection
 Breast milk
 Laboratory accidents

42. DISEASE IN HUMANS:
 Acute illness usually occurs in children
 If the primary site of infection is the eye there is unilateral
edema of eyelids and conjunctivitis - Romaña's sign –
PATHEGNOMONIC
 Furuncles (chagoma) appear at the point of entry of the
infection.
 Signs - fever, malaise, enlarged lymph nodes, liver and
spleen.
 Rarely myocarditis and meningoencephalitis

43.  The chronic phase
a) Asymptomatic (indeterminate form) - more frequent,
typically in the beginning of the chronic phase and lasting
all life in most of the patients
b) Cardiac form - 30% of the patients, with conduction
disorders, arrhythmia, cardiomyopathy, heart failure and
secondary thromboembolism
c) Digestive lesions -megaoesophagus and megacolon

44. DISEASE IN ANIMALS:
 Acute and in apparent infection - wild animals
 The acute form- fever, enlarged liver, lymph nodes and heart
irregularities
 Lasts 10-30 days – no clinical signs usually - sometimes
myocarditis occurs.
 Chronic disease in dogs.
 Lesions in dogs resemble those in humans.

45. DIAGNOSIS:
 In the acute stage, trypanosomes should be looked for by
examination of anticoagulated fresh blood for motile organisms.
 In the chronic stage, the parasite can only be detected by
culture or xenodiagnosis.
TREATMENT:
 Therapy is unsatisfactory
PREVENTION/CONTROL:
 Destroy the vector by insecticides. Use insect nets to prevent
bites. Screen blood donors

46. LEISHMANIASIS
1. Cutaneous leishmaniasis: most common
 Chiclero ulcer, pianbols, uta and buba (in theAmericas)
 Oriental sore,Aleppo boil (in the OldWorld)
 Baghdad boil, Delhi boil, Bauru ulcer (in the Middle East)
2. Visceral leishmaniasis: kala-azar -most serious
3. Mucocutaneous :espundia

47.  Cutaneous leishmaniasis
Leishmania mexicana
L.brasiliensis
L.tropica
 Visceral leishmaniasis - L.donovani,L.infantum,and L.chagasi.

49.  300 000 Estimated cases of visceral leishmaniasis (VL) and
over 20 000 deaths annually
 1 million Cases of cutaneous leishmaniasis (CL) reported in
the last 5 years.
 310 million People at risk of infection in six countries
reporting over 90%VL cases worldwide
(WHO)

50. RESERVOIRS AND INCIDENCE
 Wild animals, dogs and humans serve as reservoirs.
 Humans are the only known reservoir in India.
 The geographic distribution of the cutaneous disease is Texas,
Mexico, Central and South America, India, Pakistan, the Middle
East, southern Russia, the Mediterranean coast and Africa.
 The distribution of visceral leishmaniasis is poorly reported, but
foci probably occur in the Mediterranean basin, the Middle East,
India, China, Mexico, Central and SouthAmerica, andAfrica.

51. TRANSMISSION
 Sandfly vectors
 Congenital
 Blood-borne transmission of visceral leishmaniasis are
possible

53. DISEASE IN HUMANS:
 The primary lesion is a painful ulcer or nodule at the site of infection
with residual scarring skin and mucous membranes.
 Infiltration by inflammatory cells at the inoculation site supports the
growth of the parasite.
 Large area of chronically inflamed granulation tissue.
 The overlying skin undergoes hyperplasia and then necrosis with
spreading ulceration.
 The lesions may heal, become fibrosed or extend indefinitely to
produce considerable disfigurement.

54. Chronic skin ulcerations with raised
edges at site of sand fly bite.

55. Cutaneous leishmaniosis

57. In the visceral disease
 Intermittent irregular fever occurs with sweats, enlarged
spleen, weight loss and anemia leading to ascites, edema,
diarrhea and secondary infections.
 Dark pigmentation of the skin may occur.
 There is gross enlargement of liver and spleen.
 Without treatment, the case fatality rate is 90%.

58. Mucocutaneous leishmaniasis
 Leads to partial or total destruction of mucous membranes of
the nose, mouth and throat.

59. Post kala-azar dermal leishmaniasis
(PKDL)
 PKDL is a sequel of visceral leishmaniasis
 Appears as macular, papular or nodular rash usually on face,
upper arms, trunks and other parts of the body.
 It usually appears 6 months to 1 or more years after kala-azar
has apparently been cured.
 People with PKDL are considered to be a potential source of
kala-azar infection

60. DISEASE IN ANIMALS:
 L.mexicana causes ulcers of the skin in rodents and other wild
animals- at the base of the tail.
 L.braziliensis causes a systemic infection with few skin lesions
in wild animals. No skin lesions have been found in dogs.
 Dogs infected by L.tropica may suffer form cutaneous lesions
similar to those found in humans.
 L.donovani produces visceral lesions in dogs, with enlarged
lymph nodes, liver and spleen.

61. DIAGNOSIS:
 Definitive diagnosis is achieved by finding the parasite-either
the amastigote in stained smears or biopsies, or the motile
promastigote in culture.
 Serologic and skin tests provide only indirect evidence of
infection.
TREATMENT:
 Treatment remains inadequate because of drug toxicity, long
courses required, and frequent need for hospitalization.The
drug of choice is sodium antimony gluconate.Alternative
drugs for some forms of infection are amphotericin B and
pentamidine.

62. PREVENTION/CONTROL:
 Use insecticides in house and buildings to control the vector.
 Eliminate rubbish heaps which are breeding areas for
sandflies.
 Avoid sandfly bites by protective clothing.
 Keep dogs indoors after sundown and remove infected dogs.

63. Sarcocystosis
Intestinal sarcocystosis
 Sarcocystis hominis
 DH- Human
 IH- Cattle
Muscular sarcocystosis
 S.lindemanii
 Man dead end host
 S.suihominis
 DH- Humans
 IH- Pig

64. Epidemiology
 Worldwide, the incidence of intestinal sarcocystosis is
estimated to be 6-10%
 Approximately 20% of people in Malaysia are sero positive
 Throughout Southeast Asia, 21% of autopsy specimens
contain the parasite
 More than 60 cases have also been reported in the U.S often
as an incidental finding

65. Life cycle

66. Symptoms
 Intestinal
sarcocystosis
 IP- 3 to 6 hours
 Often asymptomatic
 Mild fever
 Diarrhea
 Chills
 Vomiting
 Respiratory problems
 Muscular sarcocystosis
 Muscle cyst
 Myalgia
 Muscle weakness
 Transitory edema

67. PREVENTION
 Intestinal sarcocystosis
 People should avoid eating raw or undercooked beef or pork
 Sarcocysts in meat can be destroyed by
 Cooking at 700C for 15 minutes
 Freezing at –40C for 2 days or freezing at –200C for 1 day
 Muscle sarcocystosis
 Food contaminated by feces or dirt should be avoided
 Good personal hygiene, such as hand washing, may also help to
prevent transmission

68. MALARIA
 Plasmodium knowlesy
 Anopheles hackeri,Anopheles balabacensis
 Parasite naturally occurring among several species of
macaques in SoutheastAsia
 Long-tailed macaque (M. fascicularis)
 Pig-tailed macaque (M. nemestrina)
 Leaf monkeys (e.g.Presbytis melalophos)
 Macaca cylopis
 The parasite has not been found in M. mulatta (rhesus
monkey) in the wild, probably because P. knowlesi in rhesus
monkey produces a fulminant and almost invariably fatal
infection

69. Asexual replication
• Fertilization and invasion of mosquito gut
• Infected cell releases sporozoites,
which migrate to the salivary glands.
Sexual replication
Exoerythrocytic
cycle
merozoites
released
"ring"
form trophozoite
ruptured
RBC releases
merozoites
schizont
Male and
female
gametocytes
Sporozoites
released from
mosquito salivary
glands invade
hepatocytes
within 30 mins.
Erythrocytic
cycle
69
Cary Engleberg

70.  Incubation period -11 to 12 days
 Mild to very severe illness
 Symptoms include fever, chills, sweats, and headache, and in
some instances, progress to serious illness including
jaundice, blood coagulation defects, shock, kidney or liver
failure, central nervous disorders and coma.

71. BABESIOSIS
 Piroplasmosis
 Babesia divergens and B.microti.
 Ixodes tick
 Babesiosis in humans is a rare intraerythrocytic infection
 Natural hosts for B. microti are various wild and domestic
animals, particularly the white-footed mouse and white-
tailed deer.

72. TRANSMISSION:
 Ixodes tick bites
 Transmission from blood transfusion
 Splenectomized, elderly, or immunosuppressed persons are
the most likely to have severe manifestations.

73. DISEASE IN ANIMALS:
 Many animals show only mild fever and recover
spontaneously.
 Hemolysis
 Enlarged spleen, liver
 Hemoglobinuric nephrosis.

74. DISEASE IN HUMANS:
 B. microti infection lasts a few weeks to a month
 Irregular fever, chills, headache, diaphoresis, myalgia, and
fatigue but is without malaria-like periodicity of symptoms.
 Hemolytic anemia, hepatosplenomegaly.
 The disease is self-limited and most patents recover without
sequelae.
 Infection with B. divergens has only been reported in
splenectomized patients
 Progresses rapidly with high fever, severe hemolytic anemia,
jaundice, hemoglobinuria, and renal failure; death usually
follows.

75. DIAGNOSIS:
 ID of the intraerythrocytic parasite on Giemsa-stained blood
smears or serology.
TREATMENT:
 B. divergens: blood transfusions, renal dialysis, pentamidine
plus trimethoprim-sulfa.
 B. microti:Treat symptomatically since most case are self-
limiting. In splenectomized patients, quinine plus
clindamycin and transfusions.

76. CRYPTOSPORIDIOSIS
 Cryptosporidium parvum- people and calves
 In recent years, C. ubiquitum, has been emerging as another
major zoonotic species that infects persons
 C hominis (formerly C parvum type I) is a specific human
pathogen

77. RESERVOIR AND INCIDENCE
 Rodents, birds (particularly turkeys and chickens), ruminants,
fish, reptiles, cats, dogs, rabbits, NHP's.
 Children over 2 years of age, animal handlers, travelers, Cattle
farmers,Veterinarians who come in contact with farm animals
 Infants and younger children in day-care centers

78.  One of the three most common diarrheal-causing pathogens in
the world
 10 billion oocysts per gram infected feces
 Can be infected by just one oocyst

79.  High burden of cryptosporidiosis among children in Indian slum
community (Rajiv Sarkar et al.,2013)
 Prevalence in children with diarrhea has been found to range from
1.1% to 18.9% in India
 Reported infection in bovines ranged from 11.32% to 69.32% in
India (Chhabra and pathak, 2012)
 Cryptosporidium antibodies were detected in the serum of 20 of
23 cats (87%) suggesting that the exposure rate may be high.

80. TRANSMISSION
 Transmission is usually fecal-oral
 Often through water contaminated by livestock mammal
feces
 Person to person transmission through feco-oral route

81. TRANSMISSION CYCLE

82.  Oocysts passed in stool are fully sporulated and infectious
 In humans and animals, the full life cycle occurs within a
single host
 Attach to the microvillus borders of enterocytes of the small
bowel and also are found free in mucosal crypts
 The host cell membrane deteriorates, leaving the parasitic
membrane in direct contact with epithelial cell cytoplasm
 Do not invade the tissues

84. Organisms attached
to an intestinal villus
Intestinal organisms
by scanning EM
39
Source Undetermined Source Undetermined

85. DISEASE IN MAN:
 In immunocompetent persons- no symptoms to mild enteritis to
marked watery without mucus or gross or microscopic blood.
 Low-grade fever, malaise, nausea, vomiting, abdominal cramps,
anorexia and weight loss
 Self-limited and lasts a few days to about 2 weeks.
 In immunologically deficient patients, the illness is characterized
by profuse (up to 15L daily), cholera-like diarrhea and by fever,
severe malabsorption, marked weight loss, and
lymphadenopathy.

86. DISEASE IN ANIMALS
 Severe watery diarrhoea in neonatal calves and lambs.
 In turkeys and chickens, the parasites are reported to occur
in the sinuses, trachea, bronchi, cloaca, and bursa of
Fabricius.
 The respiratory disease - coughing, gasping, and air sacculitis.

87. DIAGNOSIS
 Diagnosis is by detection of oocysts in stool by a variety of
flotation or concentration methods
 By mucosal biopsy, followed by special staining methods that use
modifications of an acid-fast stain
 Iodine staining
 Acid fast staining
 Fluorescein-labeled IgG monoclonal antibody

88. Iodine stain of stool Acid-fast stain of stool
42
Source Undetermined Source Undetermined

89. TREATMENT:
 No successful treatment has been developed so far.
 Supportive treatment

90. GIARDIASIS
 Most common intestinal protozoan parasite of people in the
U.S.
 The parasite occurs worldwide and is nearly universal in
children in developing countries.
 Giardia lamblia

91. RESERVOIR AND INCIDENCE:
 Humans are the reservoir for Giardia
 Dogs and beavers have been implicated as a zoonotic source
of infection
 In psittacines, the disease is commonly found in cockatiels
and budgerigars.
 Giardiasis is a well-recognized problem in special groups
including travelers, campers, and persons with impaired
immune states.
 However, Giardiasis does not appear to be an opportunistic
infection in AIDS.

92. TRANSMISSION
 Only the cyst form is infectious by the oral route;
 Trophozoites - destroyed by gastric acidity.
 Most infections are sporadic
 Fecal contamination of water or food
 Person-to-person contact
 After the cysts are ingested, trophozoites emerge in the
duodenum and jejunum. They can cause epithelial damage,
atrophy of villi, hypertrophic crypts, and extensive cellular
infiltration of the lamina propria by lymphocytes, plasma
cells, and neutrophils.

93. DISEASE IN MAN:
 Most infections are asymptomatic.
 Acute or chronic diarrhea, mild to severe, with bulky, greasy,
frothy, malodorous stools, free of pus and blood
 Upper abdominal discomfort, cramps, distention, excessive
flatus
DISEASE IN ANIMALS:
 Dogs and cats - Inapparent or produce weight loss and chronic
diarrhea or steatorrhea, which can be continuous or
intermittent, particularly in puppies and kittens.
 Calves - Feces are usually soft, poorly formed, pale, and
contain mucus. Gross intestinal lesions are seldom evident,
although microscopic lesions, consisting of villous atrophy and
cuboidal enterocytes, may be present.

94. DIAGNOSIS:
 Diagnosis is by identifying cysts or trophozoites in feces or
duodenal fluid.
 Unless they can be examined with an hour, specimens should
be preserved immediately in a fixative.
 A stool ELISA test or IgM serology are available.

95. TREATMENT:
 Tinidazole, Metronidazole (FLAGYL), quinacrine, or
furazolidone.Alternative drugs areTinidazole or albendazole.
PREVENTION/CONTROL:
 Hygiene, protective clothing, when handling animals.
 Prevention requires safe water supplies, sanitary disposal of
human feces
 Adequate cooking of foods to destroy cysts, protection of foods
from fly contamination, washing hands after defecation and
before preparing or eating foods
 Endemic areas - avoidance of foods that cannot be cooked or
peeled.

96. AMEBIASIS
 Amebic Dysentery,Amebiosis
 Entamoeba histolytica.

97. RESERVOIR AND INCIDENCE:
 The reservoir of E.histolytica is man.
 Most prevalent and severe in tropical areas
 It is estimated that there are about 50 million case of invasive
amebiasis and 40,000-100,000 deaths annually worldwide.
 In the USA, seropositive rates up to 2-5% have been reported in
some populations.
 Reported incidence of 0-31% in the feces of clinically normal
Rhesus monkeys, 2-67% in Chimps, and up to 30% in other
NHP.

98. TRANSMISSION
 Transmission may be by ingestion of infective cysts,
contaminated water or food, by flies, or fomites.
 Exists as resistant cysts or more fragile trophozoites
 Cysts are the infectious form found in the stool of
asymptomatic carriers or patients with mild disease.
 The cysts remain viable, if moist and cool for 12 days.
Remain viable for 30 days in water.
 Laboratory animal personnel are usually infected from fecal
matter transferred to the skin or clothing.

99. DISEASE IN HUMANS
 Mild to moderate colitis: recurrent diarrhoea and abdominal
cramps, sometimes alternating with constipation; mucus may
be present; blood is usually absent.
 Severe colitis: semi formed to liquid stools streaked with blood
and mucus, fever, colic, prostration.
 In fulminant cases, ileus, perforation, peritonitis, and
haemorrhage occur.
 Hepatic amebiasis: fever, hepatomegaly, pain, localized
tenderness.

100. DISEASE IN ANIMALS:
 In dogs, infection by E. histolytica is generally asymptomatic
and frequently localized in the cecum.
 Rhesus monkeys are generally resistant and usually
experience asymptomatic infection, but chronic, mild colitis
can occur.
 In chimpanzees, the infection can persist for a long time, in
most cases subclinically, but sometimes it invades the tissues
causing ulcerative colitis and hepatic abscesses.

101. Trophozoites in Ulcer with Ingested Red Blood Cells

102. DIAGNOSIS:
 Cysts or trophozoites in feacal sample
 Indirect HI for hepatic amebiasis
 Ultrasonography can locate the cyst and fine needle
aspiration is performed to find the organism.

103. Trophozoite in stool Cyst in stool

104. TREATMENT:
 May require the concurrent or sequential use of several drugs.
PREVENTION/CONTROL:
 Strict sanitation and personal hygiene, protective clothing and
gloves.
 Fecal screening of NHP.
 Protect water supply from fecal contamination.
 Usual chlorine levels don't destroy cysts. 10ppm chlorine
residual necessary to destroy cysts
 Heat to 50ºC (122ºF) kills cysts.
 Adequate cooking to destroy cysts.
 Protect food from fly contamination.

105. BALANTIDIASIS
 Balantidial dysentery
 Large ciliated protozoan, Balantidium coli.Trophozoite 50-
70 microns by 40-50 microns.

106. RESERVOIR AND INCIDENCE
 Distributed worldwide especially in the tropics
 Reservoir hosts – Swine, rats and NHP's.
 Humans, great apes, and several monkey species
 Incidence in NHP colonies - 0 to 63%
 Usually asymptomatic, but may see diarrhoea.

107. TRANSMISSION:
 Ingestion of cysts or trophozoites from infected animal or
human feces.
 Cyst is the infectious form.
 Contaminated water or food.

108. DISEASE IN ANIMALS AND MAN
 Many infections are asymptomatic and probably need not be
treated.
 Chronic
 Recurrent diarrhea, alternating with constipation
 Severe dysentery with bloody mucoid stools, tenesmus (the
constant feeling of the need to empty the bowel,
accompanied by pain, cramping, and involuntary straining
efforts), and colic may occur intermittently.

109. DIAGNOSIS:
 Use fresh fecal samples to identify trophozoites or cysts.
Trophozoites in scrapings or biopsy of ulcers of the large
bowel.
TREATMENT:
 Tetracycline or Iodoquinol
PREVENTION/CONTROL:
 Good sanitation & personal hygiene practices in NHP and
swine colonies.
 Protect water and food from fecal contamination.
 Identify positive lab animals and treat.

110. REFERENCE
 Dhumne M., Sengupta C., Kadival G., Rathinaswamy ,A.
AndVelumani A. (2007). – National seroprevalence of
Toxoplasma gondii in India. J.Parasitol., 93: 1520-1521.
 WHO ,Weekly epidemiological record, no. 7, 18 february
2005
 www.who.int

111. THANK U