majority diseases covered

1. ARTHOPOD VECTOR BORNE
DISEASES
Dr. N.Vinay Kumar
Under the guidance of Dr. J M Pawar sir

2. ARTHROPOD
• Arthropod is a Greek word meaning Jointe Leg(Arthron:joint,pod:foot)
• It is an invertebrate animal having an exoskeleton, a segmented body and paired
body appendages.
VECTOR
• A vector is an organism that does not cause disease in itself ,but does spread the
parasite to other life forms.

3. Arthopods of medical importance

5. Transmission of arthopod vector borne diseases
1)Direct contact-eg.scabies,pediculosis
2)Mechanical trasmission-eg.diarrhoes,dysentry
3)Biological transmission-3 types
a)propagative -eg.plague bacilli in ratflea
b)cyclo-developmental-eg.filarial larva in culex
c)cyclo-propagative -eg.malarrial parasite in anopheles

6. Diseases transmitted by vectors
ANOPHELES
• Malaria
• Lymphatic filariasis
CULEX
• Lymphatic filariasis
• Japanese encephalitis
AEDES
• Yellow fever
• Dengue fever
• Chikungunya
• Zika
MANSONIA
• Lymphatic filariasis
TseTse fly
• African sleeping sickness
BLACK FLY
• Onchocerciasis
SAND FLY
• Kala azar
• sand fly fever
• oryza fever
HORSE FLY
• Loiasis

7. HARD TICK
• KFD
• tick paralysis
• Tularemia
• Lyme disease
• Babeseosis
SOFT TICK
• Q fever
• Relapsing fever
REDUVID BUG
• Chagas disease
RAT FLEA
• Plague
• Endemic typhus
LOUSE
• Relapsing fever
• Epidemic typhus
• Trench fever
MITE
• rickettsial pox
• scrub typhus

8. Diseases transmitted by mosquitos
• Malaria
• Lymphatic filariasis
• Japanese encephalitis
• Yellow fever
• Dengue fever
• Chikungunya
• Zika

9. MOSQUITO

10. Malaria
• Name is derived from Italian Mal’ aria or bad air
• 1880 - Charles Louis Alphose Lavern discovered malarial parasite in wet mount.
• 1898 - Roland Ross - Life cycle of parasite transmission, wins Nobel Prize in 1902
• Malaria is a vector-borne infectious disease caused by single-celled protozoan parasites
of the genus Plasmodium.
• Malaria is transmitted from person to person by the bite of female mosquitoes.
Etiology of Malaria
Four Species known to infect Man
1 Plasmodium vivax
2 P.ovale
3 P.malariae
4 P.falciparum

11. LIFE CYCLE

12. clinical manifestations
UNCOMPLICATED MALARIA
First symptoms are non specific:
• Headache, Lassitude, Fatigue
• Abdominal discomfort, muscle and joint aches, diarrhea
• Followed by fever(irregular at first), chills, rigors, perspiration, anorexia . In some
cases palpable spleen and slight enlargement of liver are also present
• Nausea,vomiting, & orthostatic hypotension are common
Signs:
• Anemia, splenomegaly, hepatomegaly

13. SEVERE FALCIPARUM MALARIA
• Unarousable Coma / cerebral malaria, convulsions
• Renal Impairment
• Noncardiogenic pulmonary edema
• Liver Dysfunction
• Hypoglycemia
• Metabolic acidosis/acidemia
• Hematological abnormality like hemoglobinuria, normocytic anemia, bleeding,DIC
• Other complications like jaundice, extreme weakness,hyperparasitemia, impaired
consciousness
• Hypotension/shock

14. complications
• Cerebral malaria
• Renal failure
• Non cardiogenic pulmonary oedema
• Hypoglycemia
• Acidosis
• Haematologic abnormalities
• Algid malaria
• Tropical splenomegaly
• Quartan malarial nephropathy

15. CEREBRAL MALARIA
• Coma is characteristic and ominous feature of falciparum malaria
• Manifests as diffuse encephalopathy
• No signs of meningeal irritation
• Muscle tone : May be Increased/ Decreased
• Tendon reflexes : Variable, Plantars : Equivocal.
• Abdominal & cremasteric reflexes are absent
• Fundus : Retinal hemorrhages, discreet spots ofretinal opacification, papilledema,
cotton wool spots
• Convulsions :In children, usually generalised, often repeated
• Residual neurological deficit(Hemiplegia, CP, cortical blindness, deafness, impaired
cognition and learning) seen in children who survive cerbral malaria

16. Diagnosis
Clinical
• Fever, sweat, chills, headache and muscle pain
Serology
• PCR
• ELISA
Blood Film (gold standard)
• Banana-shaped intraerythrocytic gametocytes identify P. falciparum
• Enlarged erythrocytes with Schuffner’s dots are characteristics of P. vivax
• Schuffner’s dots in ovale-shaped red blood cells are characteristic of P. ovale
• Band-form trophozoites are seen in P. malariae

17. TREATMENT
All Plasmodium species except chloroquine resistant falciparum malaria
Oral Drug of Choice
• Chloroquine phosphate10 mg base/kg
(maximum: 600 mg base) then 5 mg base/kg (maximum: 300 mg base),
6 hr later,24 and 48 hr.
Parenteral Drug of Choice
• Quinidine gluconate10 mg/kg loading dose(maximum: 600 mg) over 1-2 hr, then 0.02
mg/kg/min continuous infusion until oral therapy can be started Or
• Quinine dihydrochloride 20 mg/kg loading dose over 4 hr, then 10 mg/kg over 2-4 hr q8h
(maximum: 1,800mg/24 hr) until oral therapy can be started

18. Chloroquine resistant Faliciparum Malaria
Oral Regimen of Choice
 Quinine sulfate 30 mg/kg/24 hr divided in three doses for 3-7 days (maximum:
650 mg/dose) plus Tetracycline 20 mg/kg/24 hr divided in four doses for 7 days
(maximum: 250 mg/dose).
• Mefloquine hydrochloride15 mg PO followed by 10 mg/kg PO 8-12 hours later
(maximum: 1,250 mg) for 1 day.
Parenteral
• Quinidine gluconateSame as for chloroquine-sensitive P. Falciparum
or
• Quinine dihydrochlorideSame as for chloroquine-sensitive P. falciparum.
Prevention of Relapses
Plasmodium vivax and Plasmodium ovaleOnly
• Primaquine phosphate

19. ARTEMISINS
• Artemisinin derivatives clear parasitemia morerapidly than quinine . They
are active against abroader life-cycle range of blood stage parasitesthan
quinine and they are active against gametocytes .
• Artemisinin derivatives include artesunate , artemether and artemotil.
Artesunate is thepreferred artemisinin; clinical experience with
artemether and artemotil drugs is limited and they should not be used
for treatment of severedisease.
The standard dosing regimen for intravenous artesunate consists of five
doses:
• 2.4 mg/kg as the first dose, followed by
• 2.4 mg/kg at 12 and 24 hours, followed by
• 2.4 mg/kg once daily

21. Lymphatic Filariasis
• Filariasis is the pathological condition caused by infection of filarial nematodes transmitted
by different vectors.
• Infection with 3 closely related Nematodes
1) Wuchereria bancrofti
2) Brugia malayi
3)Brugia timori
Vectors of lymphatic filariasis
The major vectors of W. bancrofti are mosquitoesof the genus Culex , Anopheles and Aedes.
The vectors of B. malayi are transmitted by Mansonia; in some areas,anopheline mosquitoes.

22. life cycle

23. Clinical manifestations
• Asymptomatic amicrofilaraemia :exposed people in endemic area do not show Mf or clinical
manifestation of disease.
• Asymptomatic microfilaraemia: blood is positive for Mf, but no symptoms. carriers.
• Stage of acute manifestation: recurrent episode of acute inflammation in lymph gland and
vessels.Filarial fever, lymphangitis, lymphadenitis,lymphoedema and epididymoorchitis.
• Stage of chronic obstructive lesion:develops 10- 15 yrs after acute attack.
mainly due to fibrosis and obstruction of lymphatic vessel, causing permanent structural
change.
Hydrocele, elephantiasis and chyluria.

24. LABORATORY DIAGNOSIS
• Samples includes :
Peripheral blood , Chylous urine, Exudate of lymph varix, Hydrocele fluid,Lymph
node biopsy, skin specimen
• Microscopic examination : It deals with the detection of microfilariae.
• Macroscopic examination : detection of adult worm ( lypmh node biopsy )
• Haematological examination : eosoinophilic count is done.
• Serological test : Complement fixation test is performed.
• Intradermal test : immediate hypersensitivity test. Filarial antigen is injected
on skin. After 30 minutes a wheal over 2 cm appears.

25. Treatment
• Diethyl carbamazepine is the drug of choice for Lymphatic filariasis.
• It is filaricidal in action.
1st day—50 mg .
2nd day---50 mg tid .
3rd day--- 100 mg tid.
4th day to 21st day– 5mg/kg /day in 3 divided doses.
• Use of tetracycline to kill the adult worm & to kill wolbachia bacteria which is having a
symbiotic relation with W.bancrofti.
• Other drugs include: Ivermectin-single oral dose-150μg/kg is used to destroy the Mf, but
not the adult worm.
• Recently evaluated drugs include Levamisole, mebendazole and centprazine.

26. JAPANESE ENCEPHALITIS
• Japanese encephalitis is a mosquito-borne viral infection.
• Japanese Encephalitis is the inflammation of brain,due to Group B Arbo virus transmitted by
Culex mosquitoes.
• It is directly affect to the central nervous system and may cause severe complications.
Agent
Group B Arbo virus in the genus group of Flaviviridae.
Host
All age groups & Both genderMore in children under 15 years of age.
vector
Culex tritaeniorhynchus,c.vishnii
reservoir
Domestic pigs and wild birds(especially herons) are reservoirs of the virus.
Incubation Period
5-15 days.

27. PATHOGENESIS

28. clinical features
1. Prodromal stage
2. Acute Encephalitic stage
3. Late stage
Prodromal stageThe onset of illness is usually
acute & the
duration of this stage is usually 1-6 days.
• Fever(38-41’c)
• Headache
• Rigors (Intensive shivering)
• GI disturbances
• Nausea & Vomiting
• Lethargy
Acute Encephalitic stage This stage begins by 3-5th
day
• High grade fever
• Nuchal rigidity
• Convulsions signs of increased ICP
• Unconsciousness
• Dystonia
• Dysphasia
• Hemiplegia
• Quadriplegia

29. Late stage
• This stage begins when activeinflammation reducedie,the temperature &
ESR touch normal.
• CNS involvement is more in this stage.
• Mental impairment
• Epilepsy
• Behavioural abnormalities.
• The average period between the onset of illness and death is about 9
days .

30. Treatment
• supportive treatment (anti pyretics,anticonvulsants,diuretics etc)
VACCINATION
3 types of JE vaccines:
1. Mouse Brain-derived Purified &Inactivated Vaccine (Nakayama or
Beijing strain of JE virus)
2. Cell Culture Derived Inactivated JE Vaccine (Beijing P-3 strain)
3. Cell Culture Derived, Live Attenuated Vaccine ( SA 14 – 14 – 2
strain of JE virus)

31. Yellow Fever
• Yellow fever is a mosquito-borne acute febrile illness accompanied by hepatic
necrosis.
• It occurs mainly in tropical Africa and Latin America.
• It does not exist in India.
• The name has been derived from ‘yellow quarantine flag’ used by the ships during
17th century to warn the presence, on board of this infection.
• Yellow fever occurs in 2 major forms: urban and jungle (sylvatic) cycle.
• In the urban cycle, man serves both as reservoir and as definitive host, the virus
being transmitted by Aedes aegypti mosquito
• In the forest or sylvatic cycle, wild monkeys act as reservoirs and several species of
forest mosquitos are vectors. Human cases occur only when humans trespass into
the forest or when monkeys raidvillages

32. Pathogenesis
• After introduction into the skin by the mosquito-bite, the virus
multiplies locally and spreads to the local lymphnodes where it
multiplies.
• From the lymphnodes, it enters the circulating blood. The virus starts
appearing in blood 3-6 days after the bite ofinfected mosquito and
viraemia lasts for 4-5 days.
• From blood, the virus becomes localised in the liver,spleen, kidney,
bonemarrow and myocardium, where it may persist for days.
• The lesions of yellow fever are due to the localization and
propagation of the virus in a particular organs.

33. Clinical features
• After an incubation period of 3-6 days, patient develops fever with
chills, headache, myalgia and vomiting.
• Most cases are mild in nature, especially in the endemic areas, in
whom the disease may present as undifferentiated fever without
jaundice.
• The pulse is usually slow despite a high temperature.
• In 15-20% of cases, the disease progresses to a more serious form with
jaundice, albuminuria, renal failure and haemorrhagic manifestations
and the patient may die of hepatic and renal failure.

34. Laboratory diagnosis
Detection of viral antigen
• Viral antigen or nucleic acid can be detected in tissue specimen using ELISA, PCR, and
immunohistochemistry
Isolation of virus
• Virus can be isolated from blood in the first 4 days after onset or from postmortem tissue
by intracerebral inoculation of mice or inoculating cell lines
Postmortem diagnosis
• There is severe midzonal degeneration, necrosis andacidophilic inclusion bodies seen in
the liver
Serology
• During first week of illness, IgM antibody can be detected by ELISA

35. Prophylaxis
• There is no antiviral drug against yellow fever
• The control of urban yellow fever can be achieved by eradicating the
vector mosquito
• Two vaccines have been developed for human use
1. The french neurotropic vaccine (Dakar) produced from infected
mouse brain.
2. 17D vaccine developed by Theiler in 1937 .
• Live attenuated vaccine “non virulent strain cultivated on chick
embryo & subsequently freeze dried”. Vaccine is stored at -25°C.
• Single dose, 0.5ml, S.C. injection.
• effectiveness start after 10days & persists for 10 years & then
reimmunization
is required.

36. VACCINATION CERTIFICATE
a. Is required from all international travelers including childrencoming
from or going to endemic areas "Yellow Fever belt".
b. Validity starts 10 days after primo-vaccination & lasts for 10 ys.
c. Validity starts on same day after re-vaccination & lasts for 10 ys.
d. If no certificate is available: traveler is isolated for 6 days from date
of leaving endemic area.

37. Dengue
• Dengue fever is clinically similar to the illness caused by the chikungunya
and O’nyong-nyong viruses.
• Dengue virus is widely distributed in the Caribbean region, south east
asia.
• In India first outbreak of dengue was recorded in 1812.
• In New Delhi, outbreaks of dengue fever reported in 1967,1970,1982,
&1996.
Morphology of Dengue virus
• spherical,Contains a single plus strand of RNA surrounded by a lipid
bilayer.
• The E (envelope), M (membrane) and C (capsid) proteins

38. Etiology types
• Four distinct antigenically related serotypes ( 1to 4) of dengue virus of the
family flaviviridae are etiologically responsible.
• Infection in human by one serotypes produces life long immunity against
re-infection by the same serotype.
• All 4 types of dengue viruses are present in India.
• Subsequent infection with other serotypes may result in a severe illness i.
e., dengue haemorrhagic fever or dengue shock syndrome.
• Dengue transmitted by infected female Aedes mosquito.

39. Pathogenesis
1.The virus is inoculated into humans with the mosquito saliva.
2.The virus localizes andreplicates in various organs,for example, local lymph nodes,
liver, spleen and the thymus.
3.The virus is then released from these tissues into theblood.
4.Via the blood, the virus spreads throughout the body to infect other lymphatic
tissues and organs, which is accompanied by symptoms.
5.The mosquito ingests blood containing the virus.
6.The virus replicates in the mosquito midgut. It then escapes into the body cavity, and
later infects the salivary glands.
7.The virus replicates in the salivary glands and when the mosquito bites another
human, the cycle continues.

40. Clinical features
• The disease may occur in two forms
1. Classical dengue fever (break-bone fever).
2. Dengue in more serious forms with haemorrhagic manifestations (DHF/DSS).
Classical dengue fever
This usually affects older children and adults
• It has relatively benign course with fever, headache, retrobulbarpain, conjunctival infection, pain in
muscles and bones,lymphadenopathy and maculopapular rash
• The fever is typically biphasic (saddle back)
• Incubation period is 5 – 8 days
• A maculopapular rash generally appears on 3rd or 4th day
• The febrile illness lasts for about 10 days after which recovery is generally complete. It is rarely fatal.

41. Other manifestations
Dengue may also occur in more serious forms, with haemorrhagic
manifestations or with shock.
• DHF/DSS remains mostly confined among children of 5 -10 years age group in
area where multiple dengue viruses cause disease.
• It appers to be hyperimmune response.
• On reinfection with a different serotype of dengue virus, antibody formed
against the first virus reacts with the second serotype virus forming immune
complexes (virus-antibody complex).
• In DHF/DSS, initial symptoms are like those of dengue fever but associated with
haemorrhagic rash, thrombocytopenia and shock

42. Clinical Case Definition for Dengue Fever
• Classical Dengue fever or Break bone fever is an acute febrile viral
• disease frequently presenting with headaches, bone or joint pain,
• muscular pains,rash,and leucopenia
Clinical Case Definition for Dengue Hemorrhagic Fever
4 Necessary Criteria:
• 1. Fever, or recent history of acute fever
• 2. Hemorrhagic manifestations
• 3. Low platelet count (100,000/mm3 or less)
• 4. Objective evidence of “leaky capillaries:”
elevated hematocrit (20% or more over baseline) ,low albumin, pleural or other effusions
Clinical Case Definition for Dengue Shock Syndrome
4 criteria for DHF
+
Evidence of circulatory failure

44. Hemorrhagic Manifestations of Dengue
petechiae, purpura, ecchymoses,Gingival bleeding,Nasal bleeding
Hematemesis, melena, hematochezia,Hematuria
Laboratory diagnosis
1)Haematological diagnosis-Thrombocytopenia (1,00,000 cells or less per
mm3),Haemoconcentration (> 20 % rise in haematocrit).
2)Microbiological diagnosis-
• Detection of antibody
• Detection of NS1 antigen
• Isolation of virus
• PCR

45. Dengue fever Management
• There is no specific antiviral treatment.
• The management is essentially supportive and symptomatic.
• The key to success is frequent monitoring and changing strategies depending on clinical
and laboratory evaluations
• Bed rest, Antipyretics or cold sponging ,Analgesics and mild sedation.
Prophylaxis
• Control measures include elimination of mosquitoes
• No effective vaccine is available
• In order to avoid the DHF/DSS in immunised persons, a live attenuated vaccine containing
all four dengue serotypes is under clinical trials

46. Chikungunya
• The virus is transmitted by Aedes aegypti.
• Chikungunya is the native name for the disease in which thepatient lies ‘doubled –up’ due to severe joint pains
• First reported Tanzania in 1952
• The virus first appeared in India 1963 when it caused extensive epidemics in Calcutta, Madras, and other areas.
• Outbreaks at irregular intervals along east coast of India and Maharashtra till 1973.
• It remained quiesent and then reappeared in 2006.
• Large outbreak in Andhra and Tamil Nadu which spread to Kerala, Karnataka and Delhi.
• There was a reemergence of the chikungunya virus in Indonesia, Schyecelles, Reunioun island of Indian ocean
and in India(2006-2007)
• due to-
1. Mutation in the E1 glycoprotein of the virus.
2. The virus was being taken up and transmitted byAedes albopiptus.

47. Cinical manifestations
Incubation period – 2-3 days
• Adults- full blown disease
• Crippling joint pains. Migratory polyarthritis mainly
affects the small joints of the hands and the wrists
• Fever – sudden onset, biphasic with a period of
remission of 1-6 days of fever
• Lymphadenopathy
• Conjuctivitis
• Rash and Hemorrhagic tendencies.
Treatment
supportive

48. ZIKA VIRUS
• Zika virus infection is a mild febrile viral illness transmitted by mosquitoes.
• The Zika virus is a member of the Flavivirus genus in the family Flaviviridae.
• It is related to dengue, yellow fever, West Nile and Japanese encephalitis,
viruses that are also members of the virus family Flaviviridae..
• It was discovered in the Zika forest in Uganda in 1947.
• The Zika virus' incubation period is about 3 to 12 days after the bite of an
infected mosquito.
• Zika virus is transmitted to people primarily through the bite of an infected
Aedes species mosquito (A. aegypti and A. albopictus).
• also transmitted From mother to child.

49. Symptoms
• Low-grade fever (between 37.8°C and 38.5°C)
• Arthralgia, notably of small joints of hands and feet, with possible swollen
joints
• Myalgia
• Headache, retro-ocular headaches
• Conjunctivitis
• Cutaneous maculopapular rash
• Post-infection asthenia which seems to be frequent.
• More rarely observed symptoms include Abdominal
pain,Diarrhea,Constipation ,mucous membrane Ulcerations, Pruritus
• According to pediatric neurologists in Brazil that some pregnant women
infected by zika virus have given birth to the babies with a birth defect called
microcephaly.

50. Diagnosis
• IgM, IgG and PCR for Zika virus.
• acute serum (taken within 5 days of symptom onset) and convalescent serum
(2–3 weeks later) should be taken. The two samples are important to rule out
false positive tests due tocross reactivity with similar viruses such as Dengue
Treatment
• There is no commercial vaccine or specific antiviral drug treatment for Zika
virus infection.
• Treatment is directed primarily at relieving symptoms using anti-pyretics and
analgesics.

51. Diseases transmitted by flies
• Kala azar
• sand fly fever
• oryza fever
• Onchocerciasis
• African sleeping sickness
• Loiasis
• Tularemia

52. LEISMANIASIS
• it is a protozoal diseases Named after Leishman - First identified the
organisms in 1901.
• Endemic in 4 states in India:
Bihar, Jharkhand,West Bengal,Uttar Pradesh.
• Group of diseases due to infection withLeishmania which is
transmitted by sandflies.
• Reservoir: man, dogs, wild rodents & foxes.
• Vector: several species of sandflies.

53. Major pathogens

54. Life cycle

55. clinical features
Incubation period: Extremely variable (10 days - 3 to 8 months – 2yrs)
Varied presentation:
• Cutaneous
• Diffuse cutaneous
• Mucocutaneous
• Visceral Leishmaniasis (Kala Azar)
cutaneous leishmaniasis
agent-L.Tropica
Typical lesion : Develops at the site where promastigotes areinjected by
the vector
• papule - papule enlarges – ulcerates

56. MUCOCUTANEOUS LEISHMANIASIS
• agentLeishmania braziliensis
• Begins with nasal stuffiness, inflammation,Ulceration of the
nasal mucosa and septum follows.
• The lips, cheeks, soft palate, pharynx and larynx may
eventually be involved, resulting in substantial
disfigurement.
VISCERAL LEISHMANIASIS (KALA AZAR)
• agent: L. donovani
• Chronic infection with fever,hepatosplenomegaly,
lymphadenopathy & anaemia.
• There is progressive emaciation & weakness with generally
fatal outcome if not treated.

57. DIAGNOSIS
• Parasite Identification-Demonstration of Leishmania bodies in stained
smear of ulcer, organ or blood
• Serology-Anti-leishmanial antibody titers
• Skin Test-Intradermal leishmanin (Montenegro) skin test
• Aldehyde test
Treatment
Antimony-containingcompounds-
• meglumine antimonate-CL,VL,MCL
• sodium stibogluconate.-CL,MCL,VL
Other drugs -
• Pentamidine:CL
• amphotericin

58. PKDL
• Some patients in India and Africa develop skin lesions following treatment,
ranging from hyperpigmented maculesto frank nodules
• Skin lesions typically appear 1 or 2 years after treatment andmay persist for as
long as 20 years.
• Persistence of lesions beyond one year is associated with highanti - leishmanial
antibody titers and negative leishmanial skintest responses
• Anti - leishmanial treatment is indicated in Indian PKDL

59. Onchocerciasis
• Onchocerciasis caused by Onchocerca volvulus a filarial worm.
• Commonly known as river blindness / Robles' disease,
• Transmitted by blackflies of the similium species flies breed in fast-
flowing streams and rivers.

60. life cycle

61. Pathology and pathogenesis
• Microfilariae released from the female worms that cause the most severe damage
• Migrating microfilariae, exclusively found in the interstitial fluids of the skin and
subdermal tissues (not thebloodstream),
• Cause
• changes in skin pigment
• loss of elastic fibers, “hanging groin,”
• severe pruritus.
• accumulation of microfilariae in the vitreous humor.
• Visual clouding, photophobia, and ultimately retinal damage result in incurable
blindness.

62. Clinical features
• Intense itching
• Depigmentation of the skin
• Elephant skin
• Blindness
• Rashes
• Lesions
• Lymphadenitis
• General debilitation
• Serious visual impairment

63. Diagnosis
• Slit-lamp examination of the anterior segment of the eye.
• Surgical removal and examination of nodules.
• Serological test.
Management
• ivermectin (mectizan) is administered as an oral dose of 150 micrograms per
kilogram(maximum 12 mg) every 6-12 months.
• Doxycycline is used to kill the wolbabchia bacteria that live in adult worms
• surgical removal of the nodules.

64. Trypanosomiasis
• caused by Trypanosoma Brucei Gambiense.
• First isolated in 1901 by Forde.
• It is endemic in West and Central Africa
• Habitat: They live in man and other vertebrate hosts. They are
parasites of connective tissue.
• Morphology- 2 forms
Vertebrate Forms-trypomastigote
Insect Forms-Epimastigotes, Metacyclic trypomastigote.

65. Life Cycle
• T. brucei gambiense passes its lifecycle in 2 hosts.
– Vertebrate host: Man, game animals, andother domestic animals.
– Invertebrate host: Tsetse fly.
• Both male and female tsetse fly arecapable of transmitting the disease
tohumans.
• Infective form: Metacyclic trypomastigote.
• Mode of transmission:– By bite of tsetse fly
• Reservoirs: Man is the only reservoirhost, although pigs and others domestic
animals can act as chronic asymptomatic carriers of the parasite.

66. Life Cycle

67. Signs and Symptoms
• Anxiety
• Mood changes
• Fever
• Headache
• Weakness
• Insomnia at night
• Sleepiness during the day (may be uncontrollable)
• Sweating
• Swollen lymph nodes all over the body
• Swollen, red, painful nodule at site of the fly bite

68. Laboratory Diagnosis
Nonspecific Findings
• Anemia and monocytosis.
• Raised ESR due to rise in gamma globulinlevels.
• Reversal of albumin:globulin ratio.
• Increased cerebrospinal fluid (CSF) pressure and raised cell count and proteins in
CSF.
Specific Findings
• Definitive diagnosis of sleeping sicknessis established by the demonstration of
trypanosomes in peripheral blood, bonemarrow, lymphnode, CSF, and chancre
fluid.
Treatment
• pentamidine
• suramin

69. Loiasis
• caused by Loa Loa.
• also known as african eye worm
• Definitive Host: human
• Intermediate Host: horsefly genus Chrysops.
Diseases
1.LOIASIS is often asymptomatic.
2. Episodic angioedema and subconjunctival
migration of an adult worm can occur.
3. Calabar swelling.

70. life cycle

71. LAB DIAGNOSIS
• Definitive diagnosis include
Detection of microfilaria in peripheral smear 12 - 2pm (diurnal periodicity)
• Isolation of adult worm from eye,Skin,Conjunctiva,subcutaneous biopsy
specimen
• High eosinophilic count
TREATMENT
• DEC 8-10mg/kg per day for 21 days
• Ivermectine or albendazole is effective in reducing filarial load
• Surgical removal of adult worm .

72. Diseases transmitted by ticks
HARD TICK
• KFD
• tick paralysis
• Babeseosis
SOFT TICK
• Q fever
• Relapsing fever

73. Kyasanur Forest Disease
• Kyasanur forest disease (KFD) is a febrile disease associated with hemorrhages caused
by an flavivirus.
• KFD virus is a member of group B togaviruses Found in India Limited originally to
Shimoga district in Karnataka.
• rats, squirrels, shrews and bats are the main reservoirs.
• Monkeys are the amplifying hosts for the virus
• Hard tickspecies of the genusHaemophysalis particularly H.spinigera and H.turtura are
the main vectors
Natural cycle
• In enzootic states the infection is maintained in small mammals and also in ticks
• When monkeys come in contact with infected ticks ,they get infected , amplify and
disseminate the infection in “hot spots ”of infection
• Humans in these hot spots are infected by bite of infected anthrophilic ticks like H.
spinigera

74. CLINICAL FEATURES
• Acute phase with sudden onset of fever, headache severe myalgia with
prostation lasting for 2 weeks.
• GI disturbances and hemorrhagic manifestations in severe cases
• Second phase characterized by mild meningoencephalitis after an afebrile
period of 7-21 days.
Diagnosis
• Diagnosis by suspicion by clinical signs and symptoms
• H/O occupation/travel in forests
• Detecting the presence of virus in blood.
• Serological evidence by haemagglutination and immunofloresence
Treatment
Conservative
• Antipyretics
• Analgesics
• Supportive therapy

75. Lyme Disease
• Causative agent: Borrelia burgdorferi
• Reservoir host: Ixodes scapularis
• Ixodes ticks have a 2-year life cycle
• Once a tick is infected, it remains infected for the rest of its life & can transmit
bacteria to other hosts whilefeeding at a later life stage
• Nymphs more likely to feed on humans than adult ticks.
Clinical Features
3 stages
Early localized stage
Early disseminatedstage
Late stage

76. Clinical Features
• Early localized Lyme disease is marked by erythema
migrans; may develop a "bullseye" appearance as
the rash enlarges; occurs in 70-80% of infected
persons .
• Early disseminated symptoms also include fatigue,
chillsand fever, headache, muscle and joint pain,
swollenlymph nodes, facial palsy, and irregular
heart beat orheart palpitations (Lyme carditis).
• Late stage symptoms include arthritis, numbness,
nervepain or paralysis, meningitis, and problems
with memoryor concentration.

77. Q FEVER
• It is caused by Coxiella burnetii.
• Obligate intracellular, gram negative bacterium.
• Q stands for Query
• Discovered in 1937 in Queensland, Australia (slaughterhouse workers).
Transmission
ticks
Inhalation (most common)
Direct orindirect contact with infected animal
Primary reservoirs
Sheep, cattle, goats

78. clinical features
• Incubation: 2 to 4 weeks
disease includes
• 50%-Asymptomatic
• Acute
• Chronic
Acute Infection
• Flu like symptoms: high fever (up to 104-105◦F), headache, sore throat,
vomiting, nausea, fatigue.
• Pneumonia with mild cough (50%)
• Less common Hepatitis, myocarditis, central nervous system complications

79. • Chronic Disease (> 6 months)
• in 1-5% of acutely infected individuals
• Pre existing heart conditions, pregnant women, immunocompromised
• Endocarditis (60-70%)
Other
• Aortic aneursyms
• Osteomyelitis
Risk to Pregnant Women
Most asymptomatic (98%)
Transplacental transmission lead to
Reported complications
• Premature birth,Low birth weight,Miscarriage,Placentitis.
• Greatest risk during 1sttrimester

80. Diagnosis
• Serology (most common method)
IFA, CF, ELISA, microagglutination
• DNA detection methods
PCR
• Isolation of organism
Treatment
Acute disease
• Doxycycline (2-3 weeks)
Chronic disease
• Doxycycline and hydroxychloroquine (~18 months)

81. Tick Paralysis
• Results from neurotoxin in tick
saliva
• Symptoms start within 2-7 days,
beginningwith weakness in both
legs progressing toparalysis
• Paralysis ascends within hours –
may leadto respiratory failure &
death
• Treatment – removal of
embedded tick

82. TULAREMIA
• Tularemia is a rare infectious disease that can attack the skin,eyes,
lymph nodes, lungs and, less often, other internal organs. Often called
rabbit fever or deer fly fever, tularemia is caused by the bacterium
Francisella tularensis.
• Ticks and deer flies are most likely to transmit the disease to humans
SIGNS & SYMPTOMS
• Ulceroglandular tularemia
• A skin ulcer that forms at the site of infection — usually an insect or
animal bite
• Swollen and painful lymph glands Fever, Chills,Headache, Exhaustion.

83. Glandular tularemia
• samesigns and symptoms of ulceroglandular tularemia, except no skin
ulcers.
Oculoglandular tularemia
• Eye pain,Eye redness,Eye swelling and discharge,An ulcer on the
inside of the eyelid.
Oropharyngeal tularemia
Fever ,Sore throat (pharyngitis),Mouth ulcers ,Vomiting, Diarrhea
Pneumonic tularemia
• Cough ,Chest pain, Difficulty breathing.

84. COMPLICATIONS
• pneumonia.
• meningitis
• pericarditis.
• osteomyelitis.
TREATMENT
• streptomycin
• gentamicin
• doxycycline
• ciprofloxacim

85. Diseases transmitted by mite,flea,louse etc
• Plague
• Trench fever
• Epidemic typhus
• Endemic typhus
• rickettsial pox
• scrub typhus

86. PLAGUE DISEASE
• Plague is a bacterial infection , which Yersinia pestis is the etiological
agent of this disease , and mostly affects lungs , lymph nodes and
blood vessels .
• TRANSMISSION
• Air droplets,Vector borne transmission,Fecal – oral transmission
TYPES OF PLAGUE DISEASE
• BUBONIC PLAGUE DISEASE
• PNEUMONIC PLAGUE DISEASE
• SEPTICEMIC PLAGUE DISEASE

88. BUBONIC PLAGUE DISEASE
• BUBO is a Greek word which is termed for swollen lymph glands.
• It is the acute inflammation and painful swellings of the lymph nodes.
• It is the most common type of plague.
• It will occur when an infected rodent or flea bites a person.
• Symptoms : sudden high fever , headache , body pain , chills etc.
PNEUMONIC PLAGUE
• It is an another type of plague , which arises from infection of the lungs , it causes coughing
and sneezing.
• Pneumonic plague is the only form of plague that can be transmitted from person to person.
• The course of the disease is rapid , unless diagnosed and treated soon enough , typically within
a few hours.
• Death may follow in one to six days.
• Symptoms : sudden pneumonia , respiratory failure , watery mucus etc.

89. SEPTICEMIC PLAGUE
• When the bacteria enter the bloodstream directly and multiply there , it is known as septicemic
plague.
• When they are left untreated , both bubonic and pneumonic plague can lead to septicemic
plague.
• Septicemic plague is the least common of their form with a mortality rate close to 100 percent.
• Symptoms : fever , chills , body pain , severe abdominal pain etc.
DIAGNOSIS
• A blood test can identify if the person have septicemic plague.
•A needle is used to take a sample of the fluid in swollen lymph nodes to identify
bubonic plague.
•Endoscopy technique can be used to identify pneumonic plague.
•By using X – ray.

90. • ANTIBIOTICS : Streptomycin ,tetracycline
• Newer generation of antibiotics :
gentamicin and doxycycline

91. TRENCH FEVER
• acute febrile illness caused by a gram-negative bacterium
known as Bartonella quintana
• Body lice (Pediculus humanus corporis) are the vectors.
• B.quintana is transmitted when an infected louse excretes
the bacterium onto the host’s skin.
• The excretion is then scratched or rubbed into the skin.

92. Clinical manifestations
• Headache
• Rash
• Mild fever
• Bone pain (mainly in shins)
• Neck and back pain
• Pain behind the eyes
• Lymphadenopathy
• Bacteremia
• Endocarditis
• Relapsing febrile illness
• (recurrent fever, usually every fifth
day)
TREATMENT
• Penicillins
• Doxycycline
• Tetracycline
• Gentamicin
• Erythromycin

93. RICKETTSIAL DISEASES
• Rickettsial diseases are considered some of the most covert
emerging or reemerging diseases.
• Hippocrates in 460 BC used the term Typhus, meaning ‘smoke’ to
describe the confused state of intellect i.e. stupor.
• Rickettsia named after HOWARD TAYLOR RICKETTS died of Typhus
fever contracted during his studies discovered Spotted fever Rickettsia
(1906).
• Commonly reported diseases in India are Scrub typhus, Murine
typhus, Indian tick typhus, Q fever.

94. Rickettsial characteristics
• Obligate intracellular parasite.
• Gram negative pleomorphic bacteria.
• Most are zoonoses spread to humans byarthropods (except Q fever).
• Cannot grow in culture media, but cultivable only in living tissue.
• No human to human transmission.
• Rickettsial infections- classification

95. Epidemic Typhus
• Rickettsial agent: - Rickettsia prowazekii
• Insect vector :- Louse
• Mammalian Reservoir :- Human, flying squirrels
• Transmission :-
• Human to human via louse vector, directly in blood,
or as the contaminated louse feces is scratched into
the bite wound, or inhalation of infected louse feces
or dust.
• Incubation period: 5-21 days

96. Symptoms:
• Acute febrile illness
• Headache
• Myalgia
Neurologic manifestations-
• Stupor, delirium
• Vasculitis
• Gangrene
• Rash : 40-80% macular, centrifugal spread,spare palms and soles
Brill –Zinsser disease
This occurs after the person recovered from epidemic
typhus and reactivation of the Rickettsia prowazekii which
remained latent for years.

97. Murine typhus/Endemic typhus
• Rickettsial agent: -Rickettsia typhi
• Insect Vector: Flea
• Mammalian Reservoir: Rodents
Transmission :-inhalation of infected louse feces or dust.
• inoculation into skin with feces of infected fleas.
• Incubation period: 1-2 weeks
Symptoms:
• Gradual onset- fever,Headache, myalgia, cough
• Rash: maculopapular rash on trunk

98. Scrub typhus
• Rickettsial agent : Orientia tsutugamushi
• Insect Vector: Mite infective larvae CHIGGERS
• Transmission :- larval forms - chiggers found in areas ofscrub vegetations.
• Common in military and Jungle warfare, farmers
• Mammalian Reservoir: -Rodents
• Incubation period: -10-12 days
Symptoms :-
• Acute onset with chills and Fever, headache, myalgia,Dry cough
• Escher- the punched out ulcer covered with
• black scab –indicates a site of the bite
• Macular rash appears around the 5th day of the bite
• Lymphadenopathy
• Lymphocytosis
• Cardiac and cerebral involvement

99. Rocky mountain spotted fever
• Rickettsial agent:- R. rickettsii
• Insect Vector: - Tick
• Mammalian Reservoir: -Rodents, dogs
• Incubation period:- 3-7 days
• Symptoms:- Abrupt onset fever, chills, headache, myalgia
• Rash : first appears in extremities, moves centripetally and
• involve palm.
• Mortality: 70% if left untreated in elderly
• Complications:- HSM, jaundice, myocarditis, uremia, ARDS

100. Rickettsial pox

101. Diagnostic Techniques
Older techniques
• Giemsa Staining Technique
• Weil-Felix Proteus Agglutination
Test
Newer techniques
• Immunological Assays
• 1. Indirect Immuno-Peroxidase /
• Immunoflouroscent assay
• 2.ELISA
• 3.PCR
• Rapid Detection Kits
• 1.Dip-S-Ticks
• 2.Scrub typhus RCT
• 3.Scrub typhus IgM / IgG Rapid
• Immunochromatographic Assay Multitest

102. WEIL-FELIX REACTION
• A Weil-Felix reaction is a type of agglutination test in which patients
serum is tested for agglutinins to O antigen of certain non-motile
Proteus and rickettsial strains (OX19, OX2, OXK)
• OX19, OX2 are strains of Proteus vulgaris.
• OXK is the strain of Proteus mirabilis.
PROCEDURE
The Weil-Felix Test can be done as either a slide or a tube test. The
antigens necessary (OX2, OX19, and OXK) can be obtained
commercially.

103. SLIDE METHOD
On a solid surface (glass slide,tile, card), a small amount (50-100 μL) of the patient’s
serum isplaced. A single drop of the desired antigen is added, and the resulting
suspension is mixedand then rotated for one minute.Visible agglutination is
indicative of a positive result, and corresponds roughly to a titre of1:20. Positive
results can be further titrated using the tube method.
TUBE METHOD
Using 0.25% phenol saline as a diluent, a series oftubes containing two fold dilutions
of patient serum aremade with a final volume of 1 mL. A drop of antigen suspension
is added to each tube, and the mixture isincubated at 50-55 °C for 4-6 hours. A
positive tubewould show visible flocculation or granulation, which is accentuated
when the tube is gently agitated. The titre corresponds to the most dilute tube in
the series that still shows positivity. Generally, a titre of ≥1:320 isconsidered
diagnostic.

104. INTERPRETATIONS IN WEIL-FELIX REACTION
• Sera from endemic typhus agglutinateOX19, OX2.
• Tick borne spotted fever agglutinate OX19, OX2.
• Scrub Typhus agglutinate OXK strain
• Test is negative in rickettsialpox, trench fever and Q-fever.
• False positive reaction may occur in urinary or other Proteus infections
• Test may be negative in 50 percent scrub typhus

106. Principles of arthropod control
1)Environmental control
• elimination of breeding places
• Filling and drainage operation
• carefully planned water management
• provision of piped water supply
• Proper disposal of refuse and other wastes
• cleanliness in and around houses.

107. 2)Chemical control
• organochlorine, organo-phosphorus and carbamate
• To avoid undue environmental pollution, replace gradually the highly persistent
compounds such as DDT with "biodegradable" and less toxic methoxychlor, abate
and dursban.
3)Biological control
• use of larvivorous fish especially Gambusia.
4)Genetic control
• sterile male technique, cytoplasmic incompatibility and chromosomal
translocations
5)Newer methods
• insect growth regulators
• chemosterilants, and
• sex attractants or pheromones

108. MOSQUITO CONTROL MEASURES
1 ANTI-LARVAL MEASURES
• Environmental control
• Chemical control
• Biological control.
2 ANTI-ADULT MEASURES
• Residual sprays
• Space sprays
• Genetic control.
3 PROTECTION AGAINST MOSQUITO BITES
• Mosquito net
• Screening
• Repellents

109. ANTI-LARVAL MEASURES
Environmental control
• “source reduction”, and comprises minor engineering methods such
as filling, levelling and drainage of breeding places; and water
management
• adequate collection,removal and disposal of sewage and waste water.
• get rid of water holding containers such as discarded tins, empty pots,
broken bottles,coconut shells and similar other artificial collections of
water.
• aquatic plants to which the larvae attach themselves should be
removed or destroyed by herbicides.

110. Chemical control
Mineral oils
• widely used are the
diesel oil, fueloil,
kerosene and various
fractions of crude oils
• application rate for oils
is 40 to 90 litres per
hectare
Paris green
• Paris green orcopper
acetoarsenite is an
emerald green, micro-
crystalline powder
practically insoluble in
water
• kills mainly the
Anopheles larva
because they are
surface-feeders.
• Recommended dose is 1
kg of actual paris green
per hectare of water
surface
Synthetic
insecticides
• Fenthion,(22-112)
Chlorpyrifos(11-16), and
Abate(56-112)
• concentration of 1.ppm
has been found to be a
very effective larvicide,
and also the least toxic

111. Biological control
• Gambusia a/finis and
• Lebister reticulatus (sometimes
known as Barbados Millions).
These fish can be used in burrow
pits, sewage oxidation ponds,
ornamental ponds, cisterns and
farm ponds.

112. ANTI-ADULT MEASURES
Residual sprays g/m2 duration
DDT 1-2 6-12 mo
Lindane 0.5 3 mo
Malathion 2 3 mo
OMS-'-33 2 3 mo

113. Space sprays
• insecticidal formulation is
sprayed intothe atmosphere in
the form of a mist or fog to kill
insects.
i) Pyrethrum extract-nerve
poison; 1 oz per 1,000 C. ft. of
space
• Residual Insecticides-malathion
and fenitrothion for Ultra low
vol. fogging

114. Genetic control
• sterile male technique, cytoplasmic incompatibility, chromosomal
translocations, sex distortion, and gene replacement.
PROTECTION AGAINST MOSQUITO BITES
• Mosquito net
• Screening
• Repellents-Diethyltoluamide (deet); for application on the skin

115. FLY CONTROL MEASURES
Environmental control
• storing garbage,kitchen wastes and other refuse in bins with tight lids,
• efficient collection, removal and disposal of refuse by incineration,
composting or sanitary landfill.
• provision of sanitary latrines, e.g., pit privies,septic tanks, water-seal
latrines and sanitary system.
• stopping open air defecation.
• sanitary disposal of animal excreta, and
• stepping up general sanitation.

116. Insecticidal control
RESIDUAL SPRAYS
• by DDT (5%), methoxychlor (5%),
• lindane (0.5%), or chlordane (2.5%) sprayed at about
• 5 litres per 100 square metres of surface; for flies resistant to
• diazinon (2%) dimethoate (2.5%), fenthion (2.5%),
• malathion (5%), or ronnel (5%) may be used.
BAITS
• Poisoned baits containing 1 or 2 per cent diazinon, malathion,
dichlorvos,ronnel and dimethoate
CORDS AND RIBBONS
• Cords and strips impregnated with diazinon, fenthion, or dimethoate

117. Space sprays
• sprays containing pyrethrin and DDT or HCH
Larvicides
• Insecticides such as 0.5% diazinon, 2% dichlorovos, 2% dimethoate or 1 % ronnel applied
at the rate of 28-56 litres per 100
Fly papers
• made by mixing 2 lbs of resin and one pint of castor oil which should be heated together
until the mixture resembles
Protection against flies
• Screening of houses, hospitals, food markets, restaurants
Health education
• Fly control campaigns require organized individual and community effort which is the
basis of a successful public health programme

118. Control of sandflies
INSECTICIDES
• single application of 1 to 2 g/m2 of DDT or 0.25 g/m2 of lindane has
been found effective
SANITATION
• removal of shrubs and vegetation within 50 yards of human
dwellings, filling upcracks and crevices in walls and floors,and location
of cattle sheds and poultry houses at a fair distance from human
habitations should receive attention

119. Control of lice
INSECTICIDAL CONTROL
• Head and crab lice : The present recommended treatment is a lotion containing 0.5 per cent
malathion. The lotion should be left on for 12 to 24 hours when the hair can be washed.
Malathion, if correctly used, will kill lice and nits. Dust containing carbaryl is also effective as
louse powder.
• Body Lice : Since lice have become resistant to DDT and HCH, a powder containing1 per cent
malathion will obviously be the treatment of choice.Dust containing carbaryl may also be used
• Personal hygiene:daily bath with soap and water is essential. Women with long hair should
wash and clean their hair frequently. Clothing, towels and sheets should be washed in hot water
and soap and pressed with hot iron.
Autoclaving of clothes and bedding insteam sterilizers may be required for body louse control.