Ricketssiaceae

2,737 views 65 slides Apr 27, 2015
Slide 1
Slide 1 of 65
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40
Slide 41
41
Slide 42
42
Slide 43
43
Slide 44
44
Slide 45
45
Slide 46
46
Slide 47
47
Slide 48
48
Slide 49
49
Slide 50
50
Slide 51
51
Slide 52
52
Slide 53
53
Slide 54
54
Slide 55
55
Slide 56
56
Slide 57
57
Slide 58
58
Slide 59
59
Slide 60
60
Slide 61
61
Slide 62
62
Slide 63
63
Slide 64
64
Slide 65
65

About This Presentation

Rickettsia, Q Fever, Typhus


Slide Content

Rickettsiaceae Dr.M.Malathi Postgraduate Department of Microbiology Chengalpattu Medical College

Synopsis Genus Rickettsia Genus O rientia Genus Ehrlichia ---------------------------------------------------------------- Genus Coxiella Genus Bartonella

Introduction Intracellular growth Transmitted by blood sucking arthropod vectors Howard Taylor ricketts (1906) – Discovered spotted fever rickettsia – died of typhus fever contracted during his studies

Characteristics Small GNB Virus like , cannot be seen under ordinary light microscope Obligate intracellular parasite

Genus Rickettsia

TYPHUS FEVER GROUP Epidemic typhus Recrudescent typhus (Brill Zinsser disease) Endemic typhus

Epidemic typhus Causative agent: R.prowazekii V ertebrate host : Humans Human body louse : Pediculus humanus corporis

Lice

Pathogenesis: Lice become infected by feeding on ricketssiaemic patients  multiply in the gut of lice  appear in feces in 3 to 5 days  infection transmitted from person to person When the contaminated louse feces is rubbed through the minute abrasions caused by scratching Occasionally by aersols of dried louse feces through inhalation or through the conjuctiva

Incubation period is 5 to 15 days Fever with chills Characteristic rash – 4 th or 5 th day Stuporous and delirious Case fatality – 40%

Eschar

Recrudescent typhus Latent infection in whom recovered from epidemic typhus Reactivation Hence no extrahuman reservoir

Endemic typhus Causative agent: R. typhi Host: Rats, Humans Vector: Flea – Xenopsylla cheopsis Pathogenesis: Rickettsia multiplies in the gut of the flea  shed in faeces  humans

Flea

Humans acquire the disease: The bite of infected fleas, when their saliva or feces is rubbed in Through aerosols of dried feces By ingesting food recently contaminated with infected rat urine or flea feces Human infection is a dead end PERSON TO PERSON TRANSMISSION DOES NOT OCCUR

SPOTTED FEVER GROUP Common soluble antigen Multiply in the nucleus as well as in the cytoplasm of host cells All transmitted by ticks except R.akari (Mite borne) Tick typhus Rickettsial pox

Tick typhus Transovarian transmission – in ticks – both vector and reservoir Larval stage or adult ticks – infective form to vertebrate hosts Transmitted to human by tick bite

Tick

Rocky mountain spotted fever – most serious type Causative agent : R.rickettsii Indian tick typhus – R.conori Tick: Rhipicephalus sanguineus

Rickettsial pox Self limited, non fatal, vesicular exanthem Similar to chicken pox Vesicular or varicelliform rickettsiosis Causative agent: R.akari Reservoir : D omestic mouse Vector : mite ( Transovarial transmission)

Pathogenesis in humans Transmitted to humans by arthropod vectors through bite or feces Ricketssaie multiply locally and enter the blood Localised chiefly in the vascular endothelial cells  thrombus formation  occlusion of vascular lumen

Clinical features : acute febrile illness, septicemia with maculopapular rash and fever The long survival of rickettsiae in various organs and lymphatic tissues in infected humans and animals is a distinctive feature in its pathogenesis.

Specimen Smears from infected tissues Blood

Morphology Pleomorphic coccobacilli Non motile , non capsulated 0.3 – 0.6 * 0.8 – 2 um Gram negative, but do not stain well Under electron microscope  three layered cell wall

cultivation Unable to grow in cell free media Growth occurs in the cytoplasm of infected cells Optimum temperature – 32 to 35deg C Cultivated in yolk sac of developing chick embryos, also grow on HeLa , Hep-2, Detroit 6 continuous cell lines

Resistance Rapidly destroyed at 56degC Destroyed at room temp also Hence when seperated from host  preserve in skimmed milk or a suspending medium containing sucrose, potassium phosphate and glutamate (SPG medium)

Antigenic structure Spotted fever rickettsiae  A, B proteins Third surface antigen  alkali stable polysaccharide  found in some rickettsiae and in some strains of the Proteus bacilli

Who am i ?

Neil Mooser Reaction R.typhi and R.prowazekii – similar When male guinea pigs are inoculated intraperitoneally with blood from a case of endemic typhus or with a culture of R.typhi  develop fever and characteristic scrotal inflammation. Scrotum enlarged and testes cannot be pushed back into the abdomen because of inflammatory adhesions between the layers of the tunica vaginalis Neil – Mooser or tunica reaction

Genus Orientia

GENUS ORIENTIA SCRUB TYPHUS (CHIGGER BORNE TYPHUS): Causative agent: Orientia tsutsugamushi First observed in Japan Vector: trombiculid mites Mite islands Humans bitten by mite larvae (Chiggers) Transovarian transmission in mites

Trombiculid mite

Zoonotic tetrad  O.tsutsugamushi , chiggers, rats and secondary and transitional forms of vegetation Incubation period – 1 to 3 weeks Characteristic Eschar , regional lymphadenopathy and maculopapular rash Three antigenic types : Karp, Gilliam and Kato

Genus Ehrlichia

GENUS EHRLICHIA Small, Gram negative, obligate intracellular bacteria Tick borne Cytoplasm of infected phagocytic cells  grow within phagosomes as mulberry like clusters  Morula

Pathogenicity : Three infections Resembles glandular fever. Causative agent is Ehrlichia sennetsu . Endemic in Japan. Causes lymphoid hyperplasia and atypical lymphocytosis . No arthropod vector. Human infection is suspected to be caused by ingestion of fish with flukes

2. Human monocytic ehrlichiosis – caused by Ehrlichia chaffeensis . Transmitted by Amblyomma ticks. Deer and rodents are reservoir hosts. Human disease with leukopenia , thrombocytopenia and elevated liver enzymes

3. Human granulocytic ehrlichiosis – either identical with or closely related to equine pathogen Ehrlichia equi . Transmitted by ticks. Deer, cattle and sheep are the suspected reservoir. Leucopenia and thrombocytopenia are seen in patients Treatment: Doxycline for ehrlichiosis

LABORATORY DIAGNOSIS OF RICKETTSIAL DISEASES

Specimens Blood for culture Tissue for culture Serum for serological tests

Direct Microscopy Light microscope  cant see individual organism, only aggregations of rickettsial particles Giemsa stain  purple coloured basophilic inclusions Machiavello stain  red coloured inclusions Immunofluorescence microscope  skin biopsies from the centre of the petechial lesions

Culture Yolk sac of embryonated hen`s eggs Male guinea pigs or mice Tissue culture

Serological test Weil felix reaction : Agglutination test in which sera are tested for agglutinins to the O antigens of certain non motile Proteus strains OX 19, OX2, OX K Due to sharing of antigen by ricketssiae and certain strain of proteus Tube agglutination test

Other serological tests Complement fixation test ELISA RIA

Molecular methods Polymerase chain reaction

TREATMENT Tetracycline Chloramphenicol Ciprofloxacin

Genus Coxiella

GENUS COXIELLA Coxiella burnetii Causative agent of Q fever ( Query) Pleomorphic bacilli Obligate intracellular pathogen Differs from rickettsia by being More resistant to heat No vector

? ? ?

Weil felix test cannot be used to diagnose Infection is from cattle , sheep and goats Zoonotic disease Bandicoot are the reservoir Transmitted to cattle by ixodid ticks Shed in milk of infected animals and transmitted to humans

Pathogenicity Human disease characterised by interstitial pneumonia Coxiella may remain latent in the tissues of patients of 2 to 3 years

Laboratory diagnosis Blood for microscopy Culture and serum for serological test PCR

Treatment Tetracycline Macrolide antibiotics

Genus Bartonella

GENUS BARTONELLA Tiny GNB Transmitted by arthropods Pathogenic strains B.bacilliformis B.quintana B.henselae

Bartonella bacilliformis Oroya fever High mortality Late sequel  verruga peruana 1885 – Medical student  Daniel Carrion  inoculated himself with material from verruga and developed oroya fever and died Carrion`s disease

Bartonella quintana First world war  trench fever or five day fever (Million of cases) No animal reservoir Transmitted by body louse Ability to grow in blood agar

Bartonella henselae Febrile illness with lymphadenopathy following a cat scratch  Cat scratch disease Isolated from the blood of patients in blood media after prolonged incubation Demonstrated in lymph node biospy smears and sections by Warthin -Starry staining

Associated with HIV infected and immunodeficient personns Bacillary angiomatosis

THANK YOU………
Tags