Epidemiology of kfd, brucellosis and leptospirosis

1. Kyasanur forest disease
Mrs. NAMITA BATRA GUIN
Associate Professor

2. HISTORY
 Heavy mortality in two species of monkeys in march
1955 in the forested area of Shimoga district of
Karnatka, led to the discovery of the disease.
 The mortality in monkeys was followed by high
incidence of acute prostrating febrile illness and few
deaths among the villagers in neighbourhood.
 Investigation resulted in the isolation of virus from
monkeys, man and ticks.
 The disease was named after the forest name
where it was first discovered and the virus was
named as KFD virus.

3. EPIDEMIOLOGICAL DETERMINANTS
 Agent: KFD virus, member of group B togaviruses.
 Natural hosts or reservoirs: Small mammals
particularly rats and squirrels are main reservoirs.
Birds and bats are less important hosts. Monkeys are
amplifying hosts of the virus.
Cattles provide Haemaphysalis ticks plentiful source
of blood which in turn leads to population explosion
among the ticks.
Man is incidental or dead-end host and plays no
part in virus transmission.

4. EPIDEMIOLOGICAL DETERMINANTS
 Vectors: atleast 15 specie of hard ticks of the genus
Haemaphysalis are known to tranmit the disease.
KFD has also been isolated from soft ticks.
 Highest no. of human and monkey infections occur in
drier months, particularly from Jan to June.
 Host factors: Age- between 20-40 years.
Sex- attack rate is greater in males.
Occupation- cultivators or those accompanying their
cattle or cutting woods.
Human activity- epidemic period correlates with the
greatest period of human activity in the forest.

5. EPIDEMIOLOGICAL DETERMINANTS
 Modes of transmission: The transmission cycles
involves mainly monkeys and ticks.
 The disease is transmitted by the bite of infective
ticks, especially nymphal stages.
 No evidence of man to man transmission.
 Incubation period: 3 - 8days.

7. CLINICAL FEATURES
 Sudden onset of fever, headache and severe
myalgia with prostration in some patients. Acute
phase lasts about 2 weeks.
 Gastrointestinal disturbances and hemorrhages
from nose, gums, stomach and intestine may occur
in severe cases.
 In several cases, mild meningoencephalitis after an
afebrile period is also observed.
This stage is characterized by return of fever,
severe headache followed by neck stiffness, coarse
tremors, abnormal reflexes and mental
disturbances.
The case fatality rate is 5%.

8. CONTROL
 Control of ticks: Spraying at hot spots i.e. areas
where monkey deaths have been reported, within
50 metres around the spot of the monkey deaths.
Restriction of cattle movement.
 Vaccination: population should be immunized with
killed KFD vaccine.
 Personal protection: By use of insect repellants,
adequate clothing. Habit of sitting or lying down on
the ground should be discouraged through health
education. At the end of day, body should be
examined for ticks and should be removed
promptly.

9. BRUCELLOSIS
(MALTA FEVER/ MEDITERRANEAN
FEVER)

10.  One of the major bacterial zoonoses.
 Occasionally transmitted by different species of
brucella group.
 The disease is characterized by intermittent febrile
attacks, with profuse sweating, arthritis and enlarged
spleen.
 Disease may last for several days, months or years.
 Disease is endemic wherever sheeps, goats, pigs and
cattle are raised in large numbers.
 Important endemic areas are: mediterranean zones,
Europe, Central Asia, Mexico and South America.
 In India, practically every state reports animal
brucellosis. It is an occupational hazard of butchers,
shepherds, farm workers and lab personnel etc.

11. HISTORY OF THE DISEASE
 It was first described more than 2,000 years ago by
the Romans and Hippocrates.
 In 1887, Dr .David Bruce, isolated the organism that
causes brucellosis from several deceased patients
from the island of Malta.
 The mid-20th century, the Brucella bacteria was
also developed for use as a biological weapon by
the United States.
 The use of brucellosis for biological warfare
purposes was later banned in 1969 by President
Nixon.

12. EPIDEMIOLOGICAL DETERMINANTS
 Agent factors: Gram-negative rod shaped
cocobacilli of the genus Brucella.
 Four species infect man: B. melitensis (goats and
sheeps), B.abortus (cattle), B.suis (pigs), B.canis
(dogs).
Brucella can live upto 8weeks in unpasteurized milk
and upto 40days in dry soil.
 Reservoir of infection: Cattle, sheep, goats,
swine, buffaloes, horses and dogs.
Infected animals excrete Brucella in the urine,
milk, placenta, uterine and vaginal discharges
particularly during a birth or abortion.
The animal may remain infected for life.

13. EPIDEMIOLOGICAL DETERMINANTS
 Host factors: human brucellosis is a disease of
adult males. Farmers, shepherds, butchers,
veterinarians and lab. Workers are at high risk.
 Environmental factors: overcrowding of herds,
high rainfall, lack of exposure to sunlight,
unhygienic practices in milk and meat production.
The infection can travel long distances in milk and
dust. Organism can survive in water, urine, feces,
damp soil and manure.
 Incubation period: 1-3 weeks but may be as long
as 6 months.

14. MODES OF TRANSMISSION
 Contact infection: by direct contact with infected
tissues, blood, urine, vaginal discharge, aborted
fetus and especially placenta.
 Food-borne infection: infection takes place
indirectly by ingestion of raw milk or dairy products
from infected animals. Fresh raw vegetables grown
in infected manure. Water contaminated with
excreta of infected animals.
 Air-borne infection: environment of cowshed is
highly infected. Infected aerosols and dust act as
mode of transmission. Brucellae may be inhaled in
slaughter houses and laboratories.

15. CLINICAL MANIFESTATION
 Acute phase : sudden onset of illness with
 swinging pyrexia, rigors and sweating.
 Arthralgia involving larger joints like: hip, knee shoulder
and ankle.
 Low back pain.
 Headache and insomnia
 Small firm hepatomegaly and splenomegaly.
 Leucopenia
Acute phase subsides within 2-3 weeks. There is severity
of illness but absence of clinical signs. If the patient is
treated with tetracycline, symptoms may disappear
quickly.
 Complications: thrombophlebitis, arthritis,
epididymo-orchitis and spondylitis

16. DIAGNOSIS
 An accurate history about travel, occupation and
animal exposure.
 Blood culture.
 Tissue biopsy from bone marrow or liver
 Other serological test.

17. DETECTION OF INFECTED ANIMALS BY RAPID
TEST METHODS
 Milk ring test: A sample of whole milk is mixed well
with a drop of stained brucella antigen (killed B.
abortus stained with hematoxylin).
 If antibodies are present in the milk, the bacilli
are agglutinated and rise with cream to form blue
ring at the top, leaving the milk unstained.
 If the antibodies are absent, no coloured ring is
formed and milk remains uniformly blue.

18. TREATMENT
 Tetracycline is the drug of choice.
 Relapse is common and is due to the difficulty in
eradicating the intracellular bacteria.
 Multidrug (two or more) antibiotic regimen is
recommended as it lowers the relapses.
 The antimicrobials most commonly used include
doxycycline (200mg/day), streptomycin (1gm/day),
rifampicin (600-900mg/day), gentamycin, tetracycline
(2gm/day) and trimethoprim-sulphamethoxazole.
 A full six-week course of antibiotics is recommended.

19. CONTROL OF BRUCELLOSIS
 In animals:
 Test and slaughter- the infected animals are
slaughtered with full compensation to farmers.
 Vaccination: with the live attenuated S19 brucella
strain. A compulsory vaccination program for endemic
areas. Systematic vaccination for the period of 7-10
years may result in the elimination of disease.
 Hygienic measures: a clean and sanitary environment
for animals, sanitary disposal of urine, feces, veterinary
care of animals and health education.

20. CONTROL OF BRUCELLOSIS
 In humans:
 Early diagnosis and treatment: drug of choice is
tetracycline. In patients with skeletal or other
complications I.M. streptomycin 1g daily in addition to
tetracycline.
 Pasteurization of milk: pasteurization of milk and milk
products. Boiling can be done in case pasteurization is
not possible.
 Protective measures: high standards of personal
hygiene, safe disposal of excreta, disposal of placenta,
discharges and fetuses from aborted animal. Wear
protective clothings.
 Vaccination: Human live vaccine for B. abortus is
available.

21. It can be prevented by
animal-disease-control
measures, avoidance of
unpasteurized dairy
products, and occupational
protective measures.

22. It can disappear if it is
eradicated from
animals.

23. LEPTOSPIROSIS

24. ABOUT DISEASE
 Leptospirosis is primarily a contagious disease of
animals, occasionally infect humans.
 It is caused by pathogenic spirochete of the genus
leptospira.
 Disease manifestations are varied and many
ranging in severity from a mild febrile illness to
severe and sometimes fatal disease.
 Its outbreaks mostly occur as a result of heavy
rainfall and consequent flooding.
 There was an outbreak in Orissa after the super
Cyclone in 1999.

25. EPIDEMIOLOGICAL DETERMINANTS
 Agents factors:
 Agent- Leptospira. Only strains of L. interrogans.
 Source of infection- leptospira are excreted in
the urine of infected animals for a long time,
often for an entire life time in cases of rodents.
 Animal reservoir: it affects wild and domestic
animals worldwide especially rodents. Most
domestic animals including cattle, sheep, goats
etc. may be infected through grazing in infected
areas.

26. EPIDEMIOLOGICAL DETERMINANTS
 Host factors:
 Age- children get more frequently infected than
the adults.
 Occupation- Agricultural and livestock farmers,
workers in rice fields, sugarcane fields
underground sewers workers, animal handlers
and vets etc. leisure time activities like swimming
and fishing also carry risk.
 Immunity: specific immunity follows infection.

27. EPIDEMIOLOGICAL DETERMINANTS
 Environmental factors:
 Leptospira shed in urine can survive for weeks in
soil and water.
 The association of poor housing, limited water
supply, inadequate method of waste disposal
add to the risk of causing disease.

28. MODES OF TRANSMISSION
 Direct contact: leptospira can enter the body
through skin abrasions or through intact mucous
membrane by direct contact with urine or infected
tissue.
 Indirect contact: through contact of broken skin
with soil, water or vegetation contaminated by urine
of infected animals, or through ingestion of
contaminated food or water.
 Droplet infection: infection may also occur due to
inhalation as when milking infected cows or goats
by breathing air polluted with droplets of urine.
 Direct man to man transmission is rare.

30. Clinical types:
 Anicteric leptospirosis
• It is the milder form of the disease.
• Patients have fever, myalgia but do not have
jaundice.
• Almost 90% of patients have this type of
illness.
 Icteric leptospirosis
• It is the severe form of the disease.
• It is characterized by jaundice and is usually
associated with involvement of other organs.
• About 5-10% of patients have these type of
manifestations

31. Anicteric Leptospirosis- Sign and
symptoms:
Fever - Patients have remittent fever with chills.
Myalgia-It is a very characteristic finding in
leptospirosis. Calf, abdominal & lumbosacral
muscles are very painful & severely tender.
Conjunctival Suffusion- There is reddish
colouration of conjunctiva.
Headache -intense,throbbing, commonly in frontal
region.
Renal manifestations
Pulmonary manifestations
Hemorrhage

32. Icteric Leptospirosis: -( Weil’s syndrome
)
This is the more severe form of leptospirosis. As the
name suggests all patients have jaundice. Patients
present with: -
• Fever
• Myalgia
• Headache
• Conjuctival suffusion
• Oliguria/Anuria and/or proteinuria
• Nausea, vomiting
• Abdominal pain

33.  Incubation period: 10 days
 Diagnosis:
 Blood culture- it takes 1-6 weeks to become
positive.
 Agglutination test- it becomes positive after 7-
10days
 IgM ELISA – useful in early diagnosis, it is
positive as early as 2 days.

34. CONTROL
 Antibiotics: penicillin is the drug of the choice. The
dosage is 6 million units I.V. daily.
 Environmental measures: reducing contamination
by rodent control and protection of workers in
hazardous occupation. Proper disposal of wastes
and health education.