2. Do not confuse with Rickets
Vitamin D or calcium deficiency that leads to soft bones

3. Zinsser, Lice And History
• In 1935, Harvard Medical School physician and researcher Hans
Zinsser traced the effects of vermin-borne disease on armies, cities
and populations. From his extensive research on head and body
lice, Zinsser stated unequivocally that "the body and head louse
carry the infection [typhus] from one human to another

4. HISTORY
• 17th-19th century
– Epidemics in Europe as a
result of war, disaster, or in
prisoners
• 1909: Transmission by lice
• 1917-1925: Russia
– Estimated 25 million cases
• End of WWII
– DDT used for control
– Vaccine developed

5. INTRODUCTION:
• Gram -ve, non-spore forming, nonmotile,
small
obligate
I/C
highly pleomorphic bacteria
• Have cell wall- Bigger than virus but
smaller than bacteria
• Have DNA and RNA
• Have an ATP transport system that
allows them to use host ATP, so
replication within the cytoplasm of
eukaryotic host cells
• Arthropod reservoirs and vectors
( e.g., ticks, mites, lice or fleas)
• Sensitive to antibiotics
Center for Food Security and Public
Health, Iowa State University, 2013

6. Properties:
 Parasites on - Lice, Fleas, Ticks Mites
colonizes the Gut
In vertebrates colonizes Vascular endothelium
and RES
 Unstable when separated from host
components.
Except - R. prowazekii & R. typhi- Able to
survive within louse feces for several weeks
 Possess all enzymes of the TCA cycle
 Glutamate- Main source of energy
 Weil-Felix test- Based on the antigenic cross
reactions among rickettsial antigens, mostly
LPS, and Proteus vulgaris strains OX19 and
OX2, and Proteus mirabilis OXK .
RICKETTSIA INSIDE
THE ENDOTHELIAL CELLS

7. Structure of Bacteria
Similar with Gram negative bacteria
Cell wall: outer membrane
peptidoglycan
lipopolysaccharide (LPS)
Microcapsule and polysaccharide
Two antigenically distinct groups:
LPS: heat-stable, cross-reactive with
somatic antigens of non-motile Proteus
species (Weil-Felix test)
Outer membrane protein: heatunstable, species-specific

8. Five genera in this class cause human diseases:
Rickettsia
Ehrlichia
Orientia
Bartonella (NOT I/C organism)
Coxiella (does NOT cause skin rash &
does NOT need arthropod vector)
Removed from group

9. Life Cycle of Rickettsia

10. Pathogenesis:
Obligate I/C organisms
Dermal target cells (fibroblasts,
macrophages, dermal dendritic cells,
and lymphatic endothelium)
Engulfed by mononuclear phagocytes in the
blood stream
Lungs and brain - lethality of rickettsioses
## Rickettsia rickettsii is the only organism in the genus that invades
beyond the blood vessel lining endothelium; they invade adjacent
vascular smooth muscle cells, particularly in arterioles

11. RICKETTSIAL INFECTIONS
Classified into groups:
1 Typhus Group
2 Spotted Fever Group
3 Scrub typhus

12. Two main groups:
The spotted
fever group
(SFG)
 Mainly associated with ticks, but
also with fleas (Rickettsia felis)
and mites (R. akari)
Typhus
group (TG)
 Associated with human body lice (R.
prowazekii) or fleas (R. typhi)
 Optimal growth temp. : 35 C
 Optimal growth temp.: 32 C
 G -C content (%): 32-33
 Polymerize actin- Move into the
nuclei of host cells - Cause spotted
fevers in humans
 Transovarial
and
transstadial
transmissions are essential
 G-C content (%): 29
 Can’t polymerize actin- Found in the
cytoplasm of host cells
 Not transmitted transovarially- Have
mammal reservoirs (humans for R.
prowazekii, rodents for R. typhi, and cats
for R. felis)

13. Typhus fever
DISEASE
Epidemic typhus/
SPECIES
R. prowazekii
VECTOR
RESERVOIR(S)
GEOGRAPHIC
DISTRIBUTION
Humans, flying
Africa, Asia, North
flying squirrel
Sylvatic typhus
Human body louse
squirrels
and South America
Rodents
Tropical and
Ectoparasites
Amblyomma ticks
Murine typhus
R. typhi
Flea
subtropical areas
worldwide

14. EPIDEMIC TYPHUS(LOUSE BORNE TYPHUS)Rickettsia prowazekii
( Von Prowazekii )
• Humans natural vertebrate hosts
• Vector - Human body louse (Pediculus
humanus corporis )
Human
Louse
Louse
Human
• Severe systemic infection & prostration
• If untreated, the mortality: 20-40%
Russia, Eastern Europe, Devastating
Epidemics in wars
• Napoleons retreat
• Russia 3 million deaths 1917 – 1921
• Major killer in concentration camps of WW II
• Brill-Zinsser Disease  recrudescent
disease
LIFE CYCLE

15. • Human body louse
– Pediculus humanus corporis
– Infective for 2-3 days
– Infection acquired by
feeding on infected person
– Excrete R. prowazekii in
feces at time of feeding
– Lice die within 2 weeks
• Louse feces rubbed into bite
or superficial abrasions
• Inhalation of feces
• Sylvatic typhus
– Flying squirrel
– 30 human cases in eastern
and central U.S.

16. Vasculitis
Skin –
rashes, DIC
& vascular
occlusion
Swollen &
necrotic
Thrombosis
of the vessels
Clinical Symptoms
Multiply in endothelial
cells of small blood
vessels
Incubation: 7-14 days
High fever, chills, headache, cough, myalgia
May lead to coma
Macular eruption
5-6 days after onset
Initially on upper trunk, spreads to
entire body
Except face, palms and soles of feet

17. Endemic Typhus
• Murine or Flea borne typhus
• Mild disease
• Rat act as reservoir
Flea
Rodent
Rodent
Flea
• Vector : Rat flea-Xenopsylla
cheopsis
• Man gets infected accidentally
• Saliva or feces rubbed on bitten
area, may lead to infection
• R.typhi & R. Prowazekii similar,
Biological & Immunological tests

18. Neill-Mooser Reaction
• Male guinea pig inoculated intra
peritioneally with blood of
patients – Fever, scrotal
swelling
•
Enlarged tests, and cannot be
pushed back.-due inflammation
and adhesions between layers of
Tunica vagina
• Test positive for R.typhi and
negative for R. prowazekii

19. Spotted fever................
DISEASE
Rickettsiosis
SPECIES
VECTOR
R. aeschlimannii Tick
RESERVOIR(S)
Unknown
GEOGRAPHIC
DISTRIBUTION
South Africa, Morocco,
Mediterranean littoral
African tick-bite
R. africae
Tick
Ruminants
Sub-Saharan Africa, West Indies
R. akari
Mite
House mice, wild
Countries of the former Soviet
rodents
Union, S. Africa, Korea, Turkey,,
fever
Rickettsialpox
North and S. America
Queensland tick
R. australis
Tick
Rodents
Australia, Tasmania
R. conorii
Tick
Dogs, rodents
Southern Europe, southern and
typhus
Mediterranean
spotted fever /
western Asia, Africa, India
Boutonneuse fever
Cat flea
rickettsiosis
R. felis
Flea
Domestic cats,
Europe, North and South
rodents, opossums
America, Africa, Asia
Cont.........

20. Spotted fever................
DISEASE
Mediterranean spotted
SPECIES
R. massiliae
VECTOR RESERVOIR(S)
Tick
Unknown
fever-like disease
GEOGRAPHIC
DISTRIBUTION
France, Greece, Spain,
Portugal, Switzerland, central
Africa, and Mali
Mediterranean spotted
R. monacensis Tick
fever-like illness
Lizards, possibly Europe, North Africa
birds
Maculatum infection
R. parkeri
Tick
Rodents
North and South America
Tickborne
R. raoultii
Tick
Unknown
Europe, Asia
R. rickettsii
Tick
Rodents
North, Central, and South
lymphadenopathy/
Dermcentor-borne necrosis
Rocky Mountain spotted
fever/ febre maculosa/
America
Brazilian spotted fever
Cont.........

21. Spotted fever................
DISEASE
Flinders Island spotted fever/ Thai
SPECIES
R. honei
VECTOR RESERVOIR(S)
Tick
tick typhus
Rodents,
GEOGRAPHIC
DISTRIBUTION
Australia, Thailand
reptiles
Japanese spotted fever
R. japonica
Tick
Rodents
Japan
North Asian tick typhus/ Siberian
R. sibirica
Tick
Rodents
Russia, China,
tick typhus
Tickborne lymphadenopathy
(TIBOLA)/ Dermacentor-borne
necrosis and lymphadenopathy
(DEBONEL)
Mongolia
R. slovaca
Tick
Lagomorph Southern and
s, rodents
eastern Europe, Asia

22. Rocky mountain spotted fever
Rickettsia rickettsii
Ticks acts as vectors &
reservoirs of Infection

24. Scrub typhus
DISEASE
SPECIES
VECTOR
Scrub
typhus
Orientia
tsutsugamushi
Larval mite
(chigger)
Scrub
typhus
Orientia chuto Unknown
RESERVOIR(S)
GEOGRAPHIC
DISTRIBUTION
Rodents
Asia-Pacific region from
maritime Russia and China
to Indonesia and North
Australia to Afghanistan
Unknown
Dubai

25. Scrub typhus
Etiology: Orientia tsutsugamushi
• Resembles Epidemic typhus except
for the ESCHAR
• Generalized lymphadenopathy &
lymphocytosis
•Cardiac & cerebral involvement may
be severe
Epidemiology
Source of infection--Rat
Route of transmission--Trombiculid mites
Eschar
Probability: Higher than 60%
Location: Axillary fossa, inguinal region,
perianal region, scrotum, buttocks and the
thigh
Appearance: an ulcer surrounded by a red
areola, is often covered by a dark scab
Susceptible population--All susceptible
Epidemic features-Tsutsugamushi triangle

26. Scrub Typhus
Important vector-borne disease, first
described in 1899 in Japan.
During World War II, this disease killed
thousands of soldiers who were stationed
in rural or jungle areas of the Pacific
theatre
The disease occurred and threatened people throughout
Asia & Australia. The range stretches from the Far-east
to the Middle-east (from Japan and Korea, Southeast Asia, Pakistan,
India, to Arab countries and Turkey). There are approx. 1 million
cases each year world-wide, & over 1 billion people at
risk

27. Scrub Typhus: A Rickettsial Disease
Pathogen: Orientia tsutsugamushi
Rickettsial bacteria
Vector: Leptotrombidium
An acute febrile, rickettsial disease
caused by a
gram-negative, rodshaped (cocco-bacillus) bacterium,
known as Orientia (Rickettsia)
tsutsugamushi.
Chigger-Mite
O. tsutsugamushi is transmitted to vertebrate
hosts (rodents-primary host & humanssecondary or accidental host) by the bite of larval
mites (chiggers) of the genus Leptotrombidium, e.
g. L. deliense, L. dimphalum, etc.

28. Pathogenesis
Inoculation
Papule maculoppular
Eschar ulcer
Invade Local
lymph node
Enlargement of
local LN
Spread by
Blood stream
General
symptoms of
intoxication
Invade Vascular
endothelium
Organ hyperaemia
Systemic lyphadenopathy

29. Miscellaneous............
GROUP
Anaplasma
DISEASE
SPECIES
VECTOR
RESERVOIR(S)
GEOGRAPHIC
DISTRIBUTION
Tick
Small mammals,
rodents, and deer
Primarily United
States, worldwide
Tick
Ehrlichosis
E. muris
Tick
Deer, dogs,
ruminants, and
rodents
Deer and rodents
Ehrlichosis
Ehrlichia
Human granulocytic A. phagocytoanaplasphilum
mosis
Human monocytic
E. chaffeensis
ehrlichosis
E. ewingii
Tick
N. mikurensis
Tick
Common in United
States, probably
worldwide
North America,
Europe, Asia
North America,
Cameroon, Korea
Europe, Asia
N. sennetsu
Trema- Fish
tode
Neoehrlichia Human
neoehrlichiosis
NeorickSennetsu fever
ettsia
Deer, dogs, and
rodents
Rodents
Japan, Malaysia,
possibly other parts
of Asia

30. Human monocytic ehrlichiosis
• Causative agents:
– Ehrlichia chaffeensis
– Ehrlichia ewingii
– Ehrlichia muris
•
Primary vector- Lone star tick (Amblyomma
americanum)
• Symptoms
–
–
Fever, headache, malaise, and myalgia
Rash is more common
• Diagnosis:
• Laboratory abnormalities
– Thrombocytopenia, leukopenia, and elevated
liver tests
•
PCR - laboratory diagnostic tool of choice
• Treatment:
– Doxycycline is the treatment of choice.

31. Clinical Information
• Onset: 5–10 days after tick bite
• Infects leukocytes
– E. chaffeensis prefers
monoctyes
– E. ewingii prefers granuloctyes
– Morulae can be identified
• Rash observed ~33% of patients
• Rash rarely seen with E. ewingii
infections
Diagnosis:
•Confirmed
–Fourfold change in IgG by
IFA in paired serum samples
–Detection of DNA by PCR
–Isolation of bacteria by cell
culture
•Supportive
–Elevated IgG or IgM by
IFA, ELISA, dot-ELISA or
other formats
–Morulae identification by
blood smear microscopic
examination

32. Why they seek attention???
Economic losses
to livestock
industries
Financial costs
to owners
- Veterinary
treatments
-Tick-prevention
programs
Animal
Rickettsioses
Mental and
emotional
distress to the
owners.

33. Common slayers for animal population ......
Species
Disease
Vector
Animal
Distribution
Anaplasma bovis
NOFEL
Amblyomma spp.,
Hyalomma spp.,
Rhipicephalus spp.
Cattle
S. America,
Africa, Iran,
India
A. marginale
Bovine
anaplasmosis/gallsickness
Various ticks
Biting insects
Cattle
Worldwide
A. ondiri
Bovine petechial fever
/Ondiri disease
Unknown
Cattle
Africa
A. ovis
Ovine/caprine anaplasmosis
Various ticks
Sheep,
goats
Worldwide
Ixodes spp.
Horses
America,
Europe
A. phagocytophilum Equine ehrlichiosis
Canine granulocytic
ehrlichiosis/anaplasmosis
Dogs
Feline granulocytic
ehrlichiosis/anaplasmosis
Cats
Pasture fever/
tick-borne fever
Ruminants

34. List is not meant to be exhaustive...........
Species
Disease
Vector
Animal
Distribution
Ehrlichia canis
Canine monocytic
ehrlichiosis
Rhipicephalus
sanguineus
Dogs
Worldwide
E. chaffeensis
Canine monocytic
ehrlichiosis
Amblyomma
americanum
Dogs
N. America
E. ewingiia
Canine granulocytic A. americanum
ehrlichiosis
Dogs
N. America,
Africa
E. ruminantium
Heartwater
Amblyomma
spp.
Cattle,
sheep, goats
Africa,
Caribbean
N. risticii
Potomac horse
fever/ Equine
monocytic
Neorickettsiosis
Digenic
trematodes
Horses
N. America

35. BOVINE ANAPLASMOSIS/GALLSICKNESS
• Cuasative organisms:
• A. marginale - Clinical
outbreaks
• A. centrale - limited
pathogenicity
• Anaplasma phagocytophilum
- Zoonotic
• Prevalence- All six
continents, especially in
tropical areas
TRANSMISSION:
Physical Vectors
• Flies
• Horse Flies
• Stable Flies
• Dear Flies
• Mosquitoes
• Instruments
• Surgical Instrumants
• Dehorning Instruments
• Castration Instruments
• Hypodermic Needles
Biological Vector
• Ticks

36. PATHOGENESIS
RBCs lysis
-Anemia
-Lack of O2 &
Nutrients in
Tissue
Calves Under • Show no Signs or Symptoms
6 Moths
Animal
remains
carrier
Up to 18
months old
Mature
Cattle
• Show only Symptoms
• Show Signs & Symptoms

37. Heartwater
Cowdriosis, Malkopsiekte,
Pericardite Exsudative Infectieuse,
Hidrocarditis Infecciosa,
Idropericardite Dei Ruminanti
Causative agent: Ehrlichia ruminantium
Geographic Distribution:
Sub-Saharan Africa
The Caribbean Islands
Not reported in Asia
Tick introduction into U.S.
possible
Animal Transmission
•Vector-borne - Amblyomma ticks
•Larvae and nymphs infected from
infected animals

38. Clinical Signs
• Incubation period: 14 to
28 days
• Four forms of disease
– Peracute (rare)
– Acute (most
common)
– Subacute (rare)
– Mild or subclinical
Acute form:
•Most common form
•Sudden fever (107oF)
•Inappetence, depression
•Tachypnea, respiratory distress
•Nervous signs
Chewing movements, eyelid
twitching, tongue
protrusion, circling, paddling
•Death in 1 week
Hydropericardium
Post Mortem Lesions
•
•
•
•
Hydropericardium
Hydrothorax
Ascites
Pulmonary & mediastinal
edema
• Congestion and edema in
the brain
Hydrothorax
Cytoplasm of capillary
endothelial cells of
infected animals

39. Diagnosis:
Clinical signs
Fever, respiratory distress, sudden
death
Presence of Amblyomma ticks
Laboratory Tests
Microscopic identification organism
PCR, IFA, ELISA
Treatment
• Early stage
– Oxytetracycline
• Late stage
– When neurological signs
occur
– Usually futile
Vaccination:
Attenuated E. ruminantium
BALL3-strain serial passage
confers solid immunity

40. NOFEL
• NOFEL (ear in local language) can
be seen in monocytes of cattle from
S. America, Africa, and the Indian
subcontinent
• Causative agent: Anaplasma bovis
• Vector:
– Multiple ticks (Amblyomma,
Hyalomma, and Rhipicephalus)
• The disease is particularly severe in
cattle stressed by rain, emaciation, or
high tick burdens

41. Characterized by:
–
–
–
–
–
fever
depression
lymph node enlargement
nasal and ocular discharge
severe lung edema, and renal necrosis
 Animals frequently shake their heads and
one or both ears are held downward over
the parotid salivary gland which is
markedly inflamed, swollen, and painful
Treatment: Tetracyclines

42. BOVINE PETECHIAL FEVER/ONDIRI DISEASE
• Etiological agent- Anaplasma ondiri
– Occurs mainly in neutrophils
• Clinical signs:
– High fever
– Hemorrhagic diathesis over 10 days
– Anemia, severe leucopenia and
thrombocytopenia
– Sudden agalactia and may abort
• Diagnosis :
– organisms in blood smears
Treatment:
– Tetracyclines are effective
– Cattle surviving infections become carriers
for many months or years
POSTMORTEM
LEISONS

43. TICK BORNE FEVER/ PASTURE FEVER
Anaplasma phagocytophilum
 Tickborne fever (TBF) is a
febrile disease of domestic and
free-living ruminants in the
temperate regions
Transmitted by hard tick-Ixodes
ricinus
Main hostsSheep and cattle,
goats and deer are also
susceptible

44. CATTLE
• Known as Pasture fever
• Dullness & depression, with a
marked loss of appetite and
milk yield
• Respiratory
distress
&
coughing
SHEEP
Main clinical sign is a
sudden fever 40.5- 42.0 C for
4-10 days
 Other signs are either absent
or mild, animals appear dull &
may lose weight
Abortions in susceptible ewes & cows, newly introduced onto tickinfested pastures
Quality of the semen of infected rams and bulls may be greatly reduced

45. Diagnosis
• Case history:
Young animals born in tickinfested areas or in older
animals newly introduced to
such area
Treatment
 Short-acting oxytetracyclines Most effective treatment
Sulfamethazine also proved
useful
• Hematologic changes
• Presence of inclusions within
granulocytes
 Organism infects eosinophils, neutrophils, & monocytes, in that order
 Cytoplasmic inclusions- Grayish blue bodies in Giemsa-stained blood
smears

46. Canine Monocytic Ehrlichiosis
Tracker dog disease
Canine haemorrhagic fever
Tropical canine pancytopaenia
The Brown Dog Tick (Rhipicephalus sanguineus)
Ehrlichia canis - usually spreads Ehrlichia canis, Ehrlichia ewingii,
and other diseases.

47. Clinical signs
• Nonspecific signs –
-Fever, Anorexia & lethargy
-Lymphadenopathy, spleenomegaly
& weight loss
Ocular signs:
Anterior uveitis, corneal
opacity, hyphema and
tortuous retinal vessels
• Vomiting, diarrhea, lameness, edema
in the hindlegs, dyspnea, & purulent
oculonasal discharge
Corneal opacity
• Bleeding disorders - Anemia, mild
epistaxis, petechiae and ecchymoses
• Death - Consequence of
hemorrhages or secondary infections

48. Diagnosis
POSTMORTEM LEISONS
• A dog with fever,
enlarged lymph nodes,
bleeding, or arthritis in
multiple joints.
• Low platelet numbers,
high globulin levels,
and mild anemia on
blood testing
Canine
thrombocytopaenia
Pancytopenia
Ehrlichia canis seen in a membrane-bound inclusions (morulae) within the cytoplasm
of a monocyte (buffy coat smear, Wright stain)

49. TREATMENT
 Doxycycline - 10mg/kg once daily for a
period of three weeks at least- Treatment
of choice for acute CME
 Imidocarb dipropionate - 5mg/kg, one
or two injections at 14 day interval, IM

50. Canine Granulocytic Ehrlichiosis (Ehrlichia ewingii)
 Disease of neutrophils
 CGE classically presents with mild
signs
 fever, lethargy, anorexia, weight loss,
vomiting, diarrhea, severe but transient
thrombocytopenia, and transient mild
nonregenerative anemia with ineffective
erythropoeisis
 Major clinical signs –
 lameness and joint swelling due to
polyarthritis
Neutrophil containing
morula of Ehrlichia ewingii
(blood smear, Wright stain)

51. Potomac horse fever /Equine monocytic ehrlichiosis
• Causative agent: Neorickettsia risticii
– Also known as Shasta River Crud and Equine
Monocytic Ehrlichiosis
– It was first described in areas surrounding
the Potomac River of Washington, D.C., in the
1980s
•
Transmission:
– Freshwater snails and aquatic insects, such as
caddisflies, mayflies, damselflies, dragonflies,
and stoneflies is a reservoir for N. risticii
 Clinical signs:
- Depression
- Loss of appetite
- Fever, followed by diarrhea

52.  Pathogenesis:
Organism multiplies inside
the
intestinal
tractColitis
Bacterial toxins gain access
to the blood stream
Laminitis, even collapse of
the circulation, abortion
in pregnant mares and
death
Treatment:
•Responds well to tetracycline
• Mild cases - oral doxycycline
•Severe cases - i/v oxytetracycline

53. EQUINE EHRLICHIOSIS/EQUINE
GRANULOCYTIC ANAPLASMOSIS
• Etiological agent: A. phagocytophilum
• Epidemiology:
– Common in California but has been reported
across the U.S, Europe & S. America
•
Vectors: Ixodes spp.
• Clinical signs:
• Most infections are subclinical
• In severe vasculitis, clinical signs evolve:
–
–
–
–
–
Fluctuating fever
Depression
Partial anorexia
Ataxia, reluctance to move & limb edema
icterus

54. • Diagnosis:
• Laboratory abnormalities
– anemia,
– leucopenia,
– thrombocytopenia, and increased bilirubin
• Morulae are readily seen in neutrophils or
eosinophils
• Can also be diagnosed using an IFA or using PCR
• Treatment:
• Oxytetracycline (7 mg/kg IV q24 hours)
• There is no vaccine, and infections are best
prevented by tick control

55. INDIAN SCENERIO: A GLIMPSE
Has been reported
from 11 states in
India:
Re-emerging
High magnitude of scrub
typhus, spotted fever and
Indian tick typhus
(Batra HV, 2007)
Jammu and Kashmir
Himachal Pradesh
Uttaranchal
Rajasthan
Assam
West Bengal
Maharashtra
Pondichery
Kerala
Tamilnadu
(Mahajan S. K, 2012)
Many cases go
undiagnosed ???
•Lack of diagnostic
tools
• Less clinical
awareness
• Lower index of
suspicion

56. Diagnosis:
Staining:
Not stained by the Gram’s method
Retain basic fuschin when stained with Gimenez methodBright red
• Initial diagnosis
– History, clinical signs
– Hematologic abnormalities
– Serum chemistry
• Definitive diagnosis
– IFA
– ELISA
– PCR
– Culture
Clinical
Signs
Blood
Smears
Serological
Biopsy
Center for Food Security and Public
Tests
Health, Iowa State University, 2013
Gene
Diagnosis

57. Diagnosis and Prevention
Microscopy
Serological Test
Breaking the infection chain
 Controlling/killing the
I/H or reservoir hosts
Inactivated vaccines
Drug therapy
 Sulphonamides are not
administered-Increasing
the penetrating of the
vessel
57

58. Different Methods of Diagnosis
Tissue cultures
In Vero cells
MRC – 5 cells

59. Older Techniques
1. Giemsa Staining Technique
:- utilizes peritoneal scrapings of infected mice.
2. Weil-Felix Proteus Agglutination Test
:-Relies on the fact that Rickettsia and Proteus OX strains have common antigens
:-Test for the presence & type of rickettsial disease based on the agglutination of X-strain
Proteus vulgaris with suspected Rickettsia in a patient’s blood serum sample
:-Commonly used in hospitals & clinics
:-This test is now being replaced by a complement-fixation test.
Weil-Felix Proteus Agglutination Test

60. Serology
Weil – Felix Test
Based on principle of Hetrophile
agglutination tests
• Non motile strains of Proteus are
selected
DISEASE
WEIL-FELIX
OX1 OX OX
9
2
K
Epidemic
typhus
++
+/-
-
• OX19,OX2,OXK
Endemic typhus
++
-
-
• Sharing alkali stable carbohydrate
antigen by some Rickettsia and
certain strains of Proteus vulgaris
OX19,OX2, and P. mirabilis
OXK
Scrub typhus
-
-
++
RMSF
+
+
-
Rickettsial pox
-
-
-
Q fever
-
-
-

61. Newer Techniques
Immunological Assays
2. Indirect Immuno-Peroxidase
(IIP)
IIP= is a modification of IFA technique that
replaces the fluorochrome with peroxidase
Slide is observed using a bright-field microscope
Staining reaction is + ve when O. tsutsugamushi
particles stain light brown.
Control
Infected

62. Newer Techniques
Immunological Assays
4. Enzyme-linked Immuno-Sorbant Assay (ELISA)
ELISA test is a technique for detecting & measuring antigen or antibody
:- One of the most reliable techniques to detect antibody
against scrub typhus infection
:- Its procedure is the principal for development of recent
rapid diagnostic kits.
Widely used in laboratories & hospitals.
Ag-Ab
complex
Optical
Density
(OD)
Reading
Ag-coated
well
1. Add antigens
2. Add mouse serum
3. Add anti-Ab
4. Add enzymesubstrate mix
5.Let colorize

63. Treatment:
• Antibiotics
– Tetracyclines
• Doxycycline
– Early treatment critical
– Prolonged therapy- In severe or
complicated cases
## Rickettsial growth is enhanced in the presence of sulfonamides
Center for Food Security and Public
Health, Iowa State University, 2013

64. What we can do?????
Queensland tick typhus
Human monocytic ehrlichosis
Japanese spotted fever
Murine typhus
North Asian tick typhus/
Siberian tick typhus
Maculatum infection
Scrub typhus
Human granulocytic anaplasmosis
Rickettsialpox
TIBOLA/ DEBONEL
Mediterranean spotted fever
Human neoehrlichiosis
Flinders Island spotted fever
Rocky Mountain spotted fever

65. Prevention and Control
• Prevent tick bites
– Wear protective
clothing
– Use insect repellents
– Remove ticks as soon as
possible
• Control tick vectors
•Remove ticks from
pets
• Acaricides
• Pets, livestock,
environment
•Biological controls
•Chemotherapy
• Immunity
Center for Food Security and Public
Health, Iowa State University, 2013