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Intermediate Microorganisms

Intermediate Microorganisms

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Published by dhainey
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Published by: dhainey on Oct 31, 2008
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INTERMEDIATE MICROORGANISMS
Dr. Rose Elaine D. Tan
RICKETTSIA
CLASSIFICATION OF THE RICKETTSIAOrder: RickettsialesFamily: Rickettsiaceae Tribe: RickettsieaeGenus RickettsiaSpecies:R. rickettsiiR. akariR. conoriR. prowazekiiR. typhiR. tsutsugamuchiR. australisR. sibericaGenus RochalimaeaSpecie:R. QuintanaGenus CoxiellaSpecie:C. burnettiGENERAL CHARACTERISTIC OF RICKETTSIA:
Small gram negative pleomorphic rods or coccobacilli
filterable, size 0.3 – 0.6µm W X 0.8 – 2µm L
obligate intracellular
cannot synthesize their own AMP
cell wall structure same with gram ( - ) bacteria
contains both RNA and DNA
replicate freely in the cytoplasm
has tropism for endothelial cell that lines the blood vesselcausing vasculitis
Genus Rickettsia are unstable extracellularly under ordinaryenvironmental conditions
C. burnetti – resistant to heat and drying
multiply & reproduce by binary fission
difficult to stain
stain used for demonstration/visualization1.Gimenez – pink – red2.Machiavello red3.Giemsa blue4.Casteda blue
growth is inhibited by antimicrobials
susceptible to Chloramphenicol & Tetracycline
require living cells for growth
can be cultured using living cell medium:1.Yolk sac developing chick embryo2.Live animal ( mice / male guinea pig )3.Tissue culture
except for R. quintana which can grow in artificial mediacontaining blood with specific nutritional requirementDisease :
Rickettsiosis
zoonotic disease which infects primarily wild animals
human are accidental host
arthropod-borne
acquired through bite of infected arthropods: lice, tick, flea, &mite
o
except Q fever (C. burnetti) which is acquired byinhalation
4 groups of diseases:
o
Spotted fever group
o
 Typhus group
o
Scrub typhus group
o
Others:
Q fever
 Trench fever
Sennetsu Rickettsiosis
Characterized by fever, headache and generalized skin rashes
except Q fever - no rashes TREATMENT : DOXYCYCLINE, TETRACYCLINE, CHLORAMPHENICOLLABORATORY DIAGNOSIS :1.Direct demonstration of organism from clinical material
2.
Isolation of organism from animal model
Infected whole blood inoculated intra-peritoneally tomale guinea pig
R. rickettsii – testicular swelling
R. prowazekii – no testicular swelling3.SerologicalSerologic Diagnosis
specific antibodies develop in response to rickettsial infection
demonstration of an immune response during convalescence
is the most widely used method of confirming clinical diagnosis
Complement-fixing antibodies are useful in identifying infectiondue to Rickettsiae in different genera and groups
serologic procedures:
o
microagglutination
o
indirect hemeagglutination
o
Microimmunoflourescent antibody test
more sensitive and specific
detect specific antibodies
used for confirmation of disease
 
Weil-Felix Reaction
Based on the cross reaction between antigens in the rickettsialorganism and Proteus polysaccharide O antigen
antibodies to the rickettsial organism will agglutinate certainnon-motile strains of Proteus (0X-19, 0X-2 & OX-K)
presumptive
low sensitivity and specificity
only 17% had been confirmed by this test
Proteus agglutinins usually do not appear until after a week of illness, thus limits their usefulness in early diagnosis
False positive: Proteus bacterial infections( UTI, bacteremia, wounds)
most widely used test in US
I. SPOTTED FEVER GROUP
basic pathologic process is a widespread vasculitis involvingthe skin, with production of a rash
more severe disease can lead to dessiminated intravascularcoagulopathy with petechial and purpuric skin manifestationa.Rocky Mountain Spotted feverb.Rickettsial Poxc.Other Tick-borne Diseases
resemble RMSF
Boutonneuse fever – R. Conorii
North Asian tick Typhus – R. sibirica
Queensland tick typhus – R. australis
 Japanese spotted fever – R. japonica
A. Rocky Mountain Spotted fever
aka: Tick-borne typhus
transmission: bite of a tick infected w/ R. rickettsii
accounts for >95% of reported cases in the US
common among children and adults
incubation period: 3-12 days
Clinical manifestation:1. cardinal features: headache, fever, diffuse myalgia,rash2. rash appears 2-4 days after onsetmaculopapular petechial hemorrhagic3. Gastrointestinal complaints, arthalgia, conjunctivitis,stiff neck,periorbital edema4. splenomegaly5. hyponatremia, thrombocytopenia6. severe disease leads to DIC with petechial & purpuricrashes7. vasculitis involving viscera (brain, heart, kidneys) canproducesignificant complications
Fatality Rate if Untreated 20-25%
Pathogenesis
o
R. ricketsii produces widespread endothelial damage thatresults in occlusion of small vessels, microthrombi,microhemorrhages, secondary fluid and electrolytechanges, and in severe cases, necrosis, shock and death
o
Kinins play a role in pathophysiology of the vasculitis andDIC
Lab Diagnosis:1.Initial diagnosis and treatment should be based onclinical grounds2.Isolation – rarely done3.Weil-Felix4.Microimmunoflourescent Antibody test5.ELISA6.PCR
 Treatment
Drug of choice – Chloramphenicol
Prevention
o
Use preventive clothing, boots and leggings
o
Use forceps for removal of ticks
o
Care should be taken during removal to preventcrushing the ticks and contaminating the fingersbecause both tick tissues and tick flees are highlyinfectious
o
NO vaccine available
B. Rickettsial Pox
agent: R. akari
mite vector:
Liponyssoides sanguineus
 (formerly
 Allodermanyssus sanguineus)
incubation period: 9-14 days
Clin. Mx:
o
reddish macular rash develops at the site of the mitebite and subsequently develops an
eschar 
whichroughly coincides with the appearance of fever,headache, chills, rigors, profuse sweating, myalgias,rhinorrhea, cough, sore throat, nausea, vomiting,and abdominal pain
o
regional lymphadenopathy
o
a papulovesicular rash (blister) that bursts andcrusts over develops 1-10 days after the escharappears and lasts for several wks
Rickettsialpox
Chickenpox
Common in adultassociated with primary escharA red papule with a vesicle inthe center dries and forms ablack escharwith surroundingindurationThe cutaneousvesicles aresurrounded by papularrings(papulovesicularrash) is usually onthe trunk and extremities; thepalms, soles, and oral mucosa mayalso be involved.
Common in childrenLacks a primary lesionThe papule turns into a vesicleon an erythematousbase andresembles a "dew drop on a rosepetal“The rash begins on the head andprogresses to the trunk, arms,and then legs
Pathogenesis:
o
Microscopically, the maculopapular rash shows amononuclear perivascular infiltrate and necrosis of epithelial cells that result in intraepidermal vesicles
Lab dx:
o
isolation of organism ( blood & vesicular fluid)
o
Weil-Felix antibodies does not appear after infection withR. akari
 TREATMENT: CHLORAMPHENICOL AND TETRACYCLINE 
C. Other Tick-borne Diseases
Found in several continents
Cause sporadic cases of mild clinical pattern
resemble RMSF
North Asian tick Typhus – R. sibirica (central Asia, Mongolia,Siberia)
Queensland tick typhus – R. australis (Australia)
 Japanese spotted fever – R. japonica (Japan)
Boutonneuse fever – R. conorii (Mediterranean, Africa, India)(aka: African tick fever, Kenya tick typhus, Indian ticktyphus)
Humans are accidental hosts
Arthropod vectors: Ixodid ticks
MOT: tick bite
incubation period varies from 6-10 days
triad of symptoms are most characteristic:
o
fever, headache, and malaise
o
erythematous papules appears on days 3-5 of theillness w/c spreads from the extremities to the trunk,neck, face, palms, and soles
o
Disease is characterized local eschars or skin lesionsat the site of the tick bite
BOUTONNEUSE FEVER
o
is transmitted by the dog tick
Rhipicephalussanguineus
o
has a characteristic rash and a distinct mark:
 
 
tache noire
(eschar or cutaneousnecrosis ) at the site of the tick bitecaused by rickettsial vasculitis ("blackspot") is pathognomonic
heals slowly over 10-20 days withoutleaving a scar
II. TYPHUS FEVER
Is a louse-bourne disease
 Typhus-group organisms are characterized by intracytoplasmicgrowth and a common, soluble, group-specific, complement-fixing antigena.Epidemic Typhus
 b.
Brill-Zinsser Diseasec.Murine Typhus
a. Epidemic typhus
Aka: Louse-bourne Typhus
etiologic agent: R. prowazekii
transmitted by infected feces of the louse usually throughscratching the skin, or sometimes by bite
o
Pediculus humanus corporis -
body louse
o
Pediculus humanus capitis – head louse
During each blood meal, the feeding process is irritating andscratching by the host produces minor excoriations thatfunction as portals of entry for the rickettsia in the louse feces
Clin Mx:
o
incubation period: 10-14 days
o
severe frontal headache, fever, malaise
o
skin rash (hallmark) 4-7 days after onset, noted atthe trunk spreading to the extremities (centrifugalspread)
o
Rash usually spares the palms, soles and face
o
patchy cutaneous erythema
maculpopapular
hemorrhagic
o
2nd week of illness the CNS becomes involved andapathy and dullness, delirium and coma
Fatality Rate if Untreated 30%
lab dx:
o
isolation of organism
o
serologic test
o
Weil-Felix reaction
o
PCR
 Treatment:
o
 Tetracycline, Chloramphenicol
o
Patients who develop circulatory and renalcomplications before receiving antibiotics may diedespite therapy
b. Brill – Zinsser disease
aka: relapsing louse-borne typhus
secondary to recrudescent R. prowazaki
the organisms appear to lie dormant, most likely in the cells of the reticuloendothelial system, until they are reactivated by anunknown stressor, multiply and cause another acute but milderinfection
Clin. Mx:
o
milder than epidemic typhus
o
Shorter duration of the disease (less than 2 weeks)
o
skin rash rarely seen
o
headache, malaise, myalgia
Lab. Diagnosis:
o
microimmunofluorescent test using IgM and IgGantibody
o
Weil-Felix agglutinins usually do not develop
c. Murine typhus
aka: endemic typhus, flea-borne typhus, rat typhus
etiologic agent: R. typhi
man is infected when, by scratching, he introduces the feces orcontents of a crushed rat-flea,
 Xenopsylla cheopis
, which hasfed on infected rat
similar to louse-borne typhus but tends to have a milder andshorter course
Clin. Mx: mild; Fatality Rate if Untreated 1-2 percent
o
Incubation period: 1-2 weeks
o
fever is less pronounced and remittent, headache isless severe
o
rash is less extensive,
o
headache, malaise, myalgia,
Lab. Diagnosis: Serology
o
Weil-Felix Reaction
 Treatment: Tetracycline, Chloramphenicol
III. SCRUB TYPHUS
aka: Chigger-borne typhus; Tsutsugamushi disease
etiologic agent : R. tsutsugamushi
endemic in Australia, Japan, Korea, India and Vietnam
vector: trombiculid mites
Larval stage of mite (chigger) – stage that feeds on vertebrae
3 major antigenic type (Karp, Gilliam, Kato)
Clin. Mx:
o
incubation period 1-3 weeks after bite of a chigger
o
sudden onset of chills, HA, fever, cough, nausea,vomiting, myalgia
o
the site of the mite bite develops a necrotic blackscab (eschar), becomes indurated and covered by ascale
o
Lymphadenopathy proximal to the eschar
o
gen. maculopapular rash appears 5-8days after
o
deterioration of mental status, pneumonia,circulatory failure
Diagnosis: Serology
o
Weil-Felix Reaction
Agglutinins to Proteus OX-K antigen appear inthe convalescent sera of many but not allpatients with scrub typhus
 Treatment: Tetracycline, Chloramphenicol
Prevention:
o
Prevent chigger bites
Wear protective clothing
Insect repellents
o
Control of mite population
Insecticides
Clearing of vegetation
Chemical treatment of the soil
IV. Q FEVER
etiologic agent: Coxiella burnetti
Q from the word “querry”
Arthropod vector: ticks
worldwide distribution
resistant to desiccation and exposure to light or temperatureextremes
Human outbreaks 2° to:
o
Consumption of infected milk
o
handling of contaminated wool or hides
o
soil contaminated by infected animal feces
o
infected straw
o
dusty clothing

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