slides+for+posting+lecture+23+ +24+skin+blood+muscle+bacterial

8/13/2019 Slides+for+Posting+Lecture+23+ +24+Skin+Blood+Muscle+Bacterial

http://slidepdf.com/reader/full/slidesforpostinglecture23-24skinbloodmusclebacterial 1/40

Skin, Blood & Muscle: Bacterial

MICR570/DJ/F12 24/25-1

Bacterial Infections of the Skin,Muscle, and Bloodstream

© DJ1

Donald Jungkind, Ph.D.Professor, Pathology and Microbiology

Director, Clinical Microbiology Lab.Thomas Jefferson University and Medical School

Philadelphi a, PA

The Organism to Remember inTypical Skin and Soft Tissue

Infection if You Only RememberOne!

© DJ2

Staphylococcus aureusGram Stain in Infection

• Gram + cocci – Clusters

© DJ3

• Often foundintracellularly i ngranulocytes. –

Arrows:• Blu e = Staph• Red = Artifact

Cultural Characteristi cs ofS. aureus

• Grows on blood agar inaerobic conditions

© DJ4

• White colony

– Sometimes becomesyellowish with age .

•Usually beta hemolytic.




MICR570/DJ/F12 24/25-2

Coagulase Test

• S. aureus positivefor production ofcatalase, and

© DJ5

. – Causes clo t

formation in rabbitor human plasma.

Staphylococcus aureus Diseases

• Epidemiology – The anterior nares are positive for S.

aureus in up to 30 % of thepopulation.

© DJ6

• When it gets into wounds it cancause severe infections .

S. aureus Alpha-tox in

• Chromosomally encoded, lowmolecular weight pro tein. – Causes necrosis o r death in

© DJ7

exper men a an ma s.• Cause mammalian cell

membranes to leak throughpores formed by toxin.

S. aureus Pyrogenic Exotoxins

• A fami ly of exotox ins – Found in certain strains of S. aureus

© DJ8

• Cause toxic effects at sites remotefrom site of infection.




MICR570/DJ/F12 24/25-4

Coagulase in Infection

• Coagulase is not a toxin, butplays role in pathogenesis – Staphylococci coated with fibrin

© DJ13

are resistant to phagocytosis.• Fibrin deposition in the area of

staphylococcal infections helpslocalize the lesion.

Other Extracellular Products

• Strains of S. aureus produce otherextracellular biologically active

© DJ14

su s ances – Hemolysins, hyaluronidase,

nucl ease, lipase, protease.

Infectivity and Pathogenesis

• Virulence is relatively low – Normally, 10 5 – 10 6 organisms are needed

© DJ15

. .• However!!

– In the presence of a suture, only 10 2

organisms wil l initiate an infection at the

site. This happens all the time inmedicine.

Staphylococcal infections:Clinical aspects

© DJ16




MICR570/DJ/F12 24/25-5

Staphylococcus Cellulitis• Infection of skin and soft

tissues.

© DJ17

Staphylococcus cellulitis

• Staph alternates between walling of fand rapid extension of infection.

© DJ18

Furuncle• Boils develop in hair follicles.

– Infection at base of eyelashgives rise to common stye.

© DJ19

Furuncle and CarbuncleInfection spreads from furuncle causing

abscesses in adjacent ti ssues. – This lesion is know n as a carbuncle

• Occurs often on the back of the neck.

© DJ20




MICR570/DJ/F12 24/25-7

Wound Infections• S. aureus : A major cause ofwound infection.

• Two sources:

© DJ25

– Patient’s ow n strain. – Nosocomial strains

spread by h ealth careworkers practicingpoor hygiene(no handwashing).

Diseases Caused byStaphylococcal Toxins

• Scalded skin syndrome – Toxin is absorbed into

the bloodstream, with

© DJ26

intraepidermaldesquamation occurs atremote sites.

• No S. aureus can beisolated from

desquamation site.

Toxic Shock Syndrome - TSS

• A l if e threatening S.aureus disease. – Characterized by high

fever vomitin

© DJ27

, ,diarrhea, sore throat,and muscle pain.

• Shock within 48 hours –

Renal and hepaticdamage.

80-100 cases i n USA

© DJ28




MICR570/DJ/F12 24/25-8

Skin Rash and StrawberryTongue in TSS

© DJ29

S. aureus Toxic ShockSyndrome Rash

• Skin rash develops fol low ed bydesquamation at a deeper level thanscalded skin syndrome.

© DJ30

Mechanism of TSS• Less than 5 % of women carry

S. aureus in vaginal flora. – One in five S. aureus pro duce TSST-1. – Combination of menstruation and high-

© DJ31

conditions for productio n of the toxin,which is absorbed from the local site.

• Non-menstrual TSS caused by staphpyrogenic exotoxin also occurs.

Deep Tissue Infection

• S. aureus can move from unnoticedskin lesion t o deep tissue infection. –

© DJ32

, , , , .• Staphylococcal pneumonia

– Always second ary to some other insul tto the lung su ch as influenza oraspiration.




MICR570/DJ/F12 24/25-9

Endocarditis Microabscessesand Vegetations of S. aureus

© DJ33

Therapy of S. aureus• Antibiot ic res is tance issues

– Most strains are currentlyresistant to penicillin G.

• Treatment of cho ice is Positive Beta-Lactamase Test

© DJ34

,oxacilli n, etc.).

• Many strains are nowresistant to methicillin. – Called MRSA

(methicilli n resistant S.

aureus)

Community Acquired MRSA• New str ain of MRSA has been established

in outpatients and is spreading in thecommunity. – Outpatient physicians have had patient

© DJ35

. – The usual outpatient antibiotics did not cover

this organism.• Uncomplicated skin infection may clear

with inci sion and drainage plus

clindamycin or doxycycline.• Serious infections or more resistant strainsneed IM or IV antib ioti cs such asvancomycin.

Vancomycin Resistant S. aureus -VRSA

• Overuse of vancomyc in has helped theemergence of vancomycin resistance. – VRSA strains have occasionally been

found in the world includin the USA.

© DJ36

• True VRSA can be detected by n ormal in -vitro tests.

– When a VRSA is found i n a hospital, the patientis placed in the strictest of isolation.

– Dedicated personnel may care for the patient sothat chance of transmission i s minimized. – Government agencies get involved.




MICR570/DJ/F12 24/25-10

Vancomyci n Intermediate S. aureus – VISAVISA Heterogeneous Variety -hVISA

• Vancomycin treatment failures are morecommon than for fully susceptiblestrains. – Up to 6% of the S. aureus strains may be

© DJ37

hVISAs in s ome hospitals.• Today, these strains affect more patients

than normal VRSA – VISAs and hVISAs are harder to detect

in laboratory testing than VRSA, andare often missed.

Coagulase NegativeStaphylococci

• Once thought tobe an insign ificant

© DJ38

finding in aculture report.

Coagulase NegativeStaphylococci

• Normal commensals – Skin, anterior nares, ear canals, and

mucou s membranes of humans.

© DJ39

• These organisms normally lackmajor virulence factors o f S. aureus . – Not beta-hemolytic. – Were grouped with “ normal flora”.

One Coagulase NegativeStaphylococcus Species Causing

Infection s Similar to S. aureus• S. lugdunensis

– A primary pathogen l ike S. aureus

© DJ40

• Has some characteristics of S. aureus . – Causes occasional very serio us

infections.• Abscess fo rmation• Seems to be found more frequently.

– Emerging pathogen.




MICR570/DJ/F12 24/25-12

Clinical Signif icance ofCoagulase Neg. Staph.

• More likely to be significant if: – Present in multiple blood cultures. – Intracellul ar Gram-posit ive cocc i are

© DJ45

. – Culture show s moderate to heavy

numbers on culture plates from w oundspecimens.

• Less likely to be significant:• Negative plates with bro th cultu re only

show ing as positive = very low #’s.

Deep Tissue Infection

• S. aureus can move from (unnoticed)skin lesion t o deep tissue infection. – Bone oints liver lun s other tissues.

© DJ46

, , , , .• Staphylococcal pneumonia

– Always second ary to some other insul tto the lung su ch as influenza oraspiration.

Coagulase Neg. StaphylococcusProsthetic Joint Infection

• Surgery to removeinfected prosthetic

jo in t: – Shows effect of

© DJ47

bacterial biofil m – White material is pus

containing WBC andbacteria.

– Painful joint neverfully heals. Monthsto show full effect.

Introduction: BasicCharacteristics of Streptococci

• Part of normal flora in mammals. – Inhabit oral cavity

© DJ48

– Gastroin testinal and genital tract• Some species and strains are highly

pathogenic in specific grow th

environments within the body.




MICR570/DJ/F12 24/25-13

Gram Stain

• Gram posi tivecocci in chains.

© DJ49

– Become Gramvariable as cul tureages and cells die.

Classification of Streptococci

• Based on type ofhemolysis on blood

© DJ50

. – Beta streptococcus is

shown.• If RBCs had no

hemolysis, it is: – Nonhemolytic

Pyogenic Streptococci• Streptococci that form pus

– Beta-hemolytic streptococci• Frequently cause purulent infections

© DJ51

Group A Streptococcus(Streptococcus pyogenes )

• Historically

© DJ52

– A common cause of ser ious in fection s• Causes variety of infectiou s syndrom es




MICR570/DJ/F12 24/25-14

Group A Toxin

• Pyrogenic exotoxin (SPE) – Once called erythrogenic tox in – Stimulates c tokine release causin

© DJ53

multiple effects.• Makes a red rash on skin

– Scarlet fever • Minority of strains carry this toxin.

– Toxin carried on a phage.

Famous People Who Died fromGroup A Strep Infection

© DJ54

Group A Streptococcal DiseaseEpidemiology: Pharyngitis

• Common bacterial infection of throat.

© DJ55

– Carrier rate in untreated cases• 1-4 weeks or mo re after infection

– Organism in th roat, sometimes anus.

• 2-10 % of po pulation m ay be carriers.• Spread by di rect contact or aerosols.

Scarlet Fever

• Strep throat with a characteristic rash – Deep red color :

• Cheeks, temples, buccal mucosa .• “ ”

© DJ56

– Punctate hemorrhages on palates. – “ Sandpaper” rash on trunk, arms, legs

• Rash due to toxin.




MICR570/DJ/F12 24/25-15

Punctate Hemorrhages onPalate

© DJ57

Scarlet Fever vs. Measles

© DJ58

Strawberry Tongue ofScarlet Fever

© DJ59

Poststreptococcal Sequelae• Acut e rheumati c f ever

– Inflammatory disease•

© DJ60

, , ,migratory polyarthritis

– Heart valv e damage• Murmurs, cardiac enlargement.• Repeat infections lead to prog ressive

damage.




MICR570/DJ/F12 24/25-16

Acute Glomerulonephritis

• Disease of childhood – Lesions of glomeruli.

© DJ61

• ccurs ays a er resp ra oryinfection. – Recovery after weeks or months.

• Occasional renal failure and death. – Pathogenesis: immunologic

mechanism• Ant ig en-an tibo dy co mp lex es in ki dney

Impetigo• Group A strep infection of skin.

– Infection starts at insect bite or minorabrasion.

– May co-infect wi th S. aureus .

© DJ62

• Lesions – Small vesicles with erythema – Become pustular and later crusted.

• Glomerulonephritis a complication

Group A Strep Impetigo

© DJ63

Ecthyma Strep Group A

© DJ64




MICR570/DJ/F12 24/25-17

Wound and Burn Infections

• Spreads rapidly to adjacenttissues. – Bacteremia.

© DJ65

• n ec on o s n gra s resu s nfailure of graft. – Risk of death wi th systemic

progression of infection.

Human Bi te Group A StrepInfection

© DJ66

Erysipelas• Group A streptococcal

infection of skin andsubcutaneous tissues. – Spreading area of

erythema and edema.

© DJ67

• Rapidly advancingedges.

• Often on face. – Pain, fever,

lymphadenopathy.

Streptococcus pyogenes CellulitisMay be deadly if untreated.

© DJ68




MICR570/DJ/F12 24/25-19

Vascular Compromise in Strep AToxic Shock Syndrome

© DJ73

Desquamation Strep Toxic Shock

© DJ74

Laboratory Diagnosis of BetaStreptococcus Infections

• Systemic infections –

© DJ75

– Blood cultures – Wound cultures

Group B Streptococci (GBS)Streptococcus agalactiae

• Up to 30 % of women carry GBS

© DJ76

. – Neonate can acquire GBS during

passage through birth canal

unless preventative measures aretaken.




MICR570/DJ/F12 24/25-20

Clinical Manifestations

• Neonatal disease – Lethargy, fever, sepsis, mening itis,

respiratory distress.

© DJ77

• Older children and adults – Puerperal fever at delivery – Gynecologic surgery infections – Skin and soft tissue infections.

Other Pyogenic Streptococci• Beta strep, NOT groups A or B

– Groups C and G may causepharyngitis.

• No post in fection sequelae.

© DJ78

– n an so t t ssue n ect ons• Infections of w ounds• Occasional bacteremias

– Differentiation of groups no t necessary• Treatment same as for g roups A & B

Viridans streptococci• Alpha hemolyt ic s tr eptococcus

– The term “ viridans” streptococci refersto all other alpha streptococci once S.pneumoniae has been ruled out.

© DJ79

• Pseudonym avoids speciating theseveral members of this group . – Speciation not usually c linically

required.• Speciation for positives fro m multiple

blood cultures helps prove significance – Normal flora of mouth, gut, moist skin.

Viridans Streptococcus Species• S. mil leri group

– Noted for deep tissu e abscesses.• Many species cause subacute

bacterial endocarditis .

© DJ80

– S. mutans• Also causes den tal car ies .

– S. miti s –

S. salivarius plus many others.• Detect with blood cult ures• Treat with penicilli n for weeks.




MICR570/DJ/F12 24/25-21

Streptococcus mutans

• Assoc iated w ith dental caries.

© DJ81

Viridans Streptococcus onHeart Valve

• Organisms initiallyadhere to tinyimperfections on valve.

• Treatment of endocardi tis

© DJ82

– Usually very sensitive topenicillin G if given forprolonged periods.

• Prophylaxis – Penicilli n given prior to

dental procedures in those

with damaged valves canprevent endocarditis.

Abiotrophia sp .: NutritionallyDeficient Streptococci

• Will not grow on ordinary blood agar – Requires a specific vitamin or nut rient

provided by other bacteria, or by

© DJ83

. – Colony resembles viridians or non-

hemolytic streptococcus species.• Causes bacterial endocarditi s

– Sometimes diffi cult to detect by cultureunless lab thinks to add a “ feedercolony” or special nutrients to media.

Abiotrophia Colonies AroundFeeder Colony of S. aureus

© DJ84




MICR570/DJ/F12 24/25-22

Enterococcus

• Gram positi ve cocci in chains. – Once were non-hemolytic members of

© DJ85

.• Natural habitat is th e gut.

– Very resistant to bile salts, acid, NaCl – Classified as non-hemolytic strep – Classified as Group D streptoco ccus

Species of Enterococcus• Several species exist .• Major pathogens

– E. faecalis

© DJ86

• Usually the most common clinicalisolate.

– E. faecium – the bad one .• Resistant to ampicillin• More likely to be resistant to

vancomycin than E. faecalis .

Enterococcus Diseases• Opportunistic infections

– Cause infection after broad spectrum antibiotics suchas cephalospori ns and gentamicin wip e out normalflora.

• Wound and soft tissue infections.• Bacteriemia related to indwelli ng lines

© DJ87

• (Urinary tract infections)• Wound infections in int ensive care units.

– Often a “me-too” organism in wounds. A mixture ofbacteria causing infection.

• Enterococcus plus E. coli• Enterococcus pl us anaerobes.

Resis tance and Treatment• E. faecium

– Resistant to ampicillin – Resistance to vancomycin (VRE) is

common now i n hospital acquired

© DJ88

infections.• Control wi th handwashing, employee

education, good cleaning of rooms

between patients. Reducing u se ofvancomycin.




MICR570/DJ/F12 24/25-23

Corynebacterium Characteristics

• Gram positive rods,not acid fast. – Pleomorphic shapes

© DJ89

• Coccobacilli• Irregular rods

– Clubbed ends on rods• Sometimes look like

“ Chinese letters”

Clinical Relevance• Pathogens

– Corynebacterium diphtheriae• Opportunistic pathogens

– Corynebacterium ulcerans

© DJ90

• n n ec ons – Corynebacterium jeikeium (JK)

• Nosocomial bloodstream and woundinfections

• Other species non-pathogens:

– Diphtheroids , rarely cause disease.

Corynebacterium diphtheriae

• No only a cause of diphtheria.• Causes impetigo-like skin lesions

–

© DJ91

. – Occasionally in American Indians.

• Rarely fatal

Diagnosis of Diphtheria

• Special culturerequired: – Blood agar (shown):

© DJ92

• Specialty agarsnot show n are: – Tellurite agar

– Loeffler’s agar




MICR570/DJ/F12 24/25-25

Anaero bic In fec tions are OftenMixed Gram Positive and Negative

• Anaerobesusually cause

© DJ97

infections. – Mixed with other

anaerobes orwith facultativeorganisms.

Normal Anaerobic Flora• Anaerobes colonize oxygen

deficient areas of the body. – Anaerobes predominate:

© DJ98

– Anaerobes are a major part of flora:

• Mouth, throat, upper GI• Vaginal (genital) tract• Skin (sebaceous g land)

Opportunistic AnaerobicConditions Allow Infection

• Tissues devitalized by: – Trauma

© DJ99

–

– Inflammation – Impaired blood supply

– Surgery – Foreign body

For Anaerobic Cultures:• Accep tab le Specimens

– Must decide clinically whetheranaerobes are likely to be present,then collect:

© DJ100

• Abscess fluid aspi rates.• Surgically removed tissue.• Blood cultures.




MICR570/DJ/F12 24/25-26

Clostridium perfringens

• General characteristics – Gram positive spore forming rod.

• No spores are seen in st ains of tis sue.

© DJ101

– as gro w ng anaero c ermen er • Generates large amounts of H 2 & CO 2

– Encapsulated and non -motile. – Found in colon and soil.

Clostridium perfringens Features

• Culturecharacteristics – Double zone of

hemolysis on

1 2

© DJ102

blood agar (1) – Litmus milk

stormyfermentation (2)

– Easy to identifybiochemically

Clostridium perfringens Toxins• Alpha toxin: Main pathogenic facto r

– Diffuses through tissue killing cells thusproducing more necrotic growth areasfor organism

© DJ103

• Theta toxin – Toxic for heart muscle & capill aries. – Similar to Streptolysin O in beta strep

• Enterotoxin – Causes food p oisoning.

C. perfringens: OtherMechanisms of Pathogenesis

• Fermentation of mu sclecarbohydrate – Produces crepitation

(palpable gas).

© DJ104

• Destructi ve extracellularenzymes: – Collagenase – DNAse – Hyaluronidase – Protease

Gas




MICR570/DJ/F12 24/25-27

Gas Gangrene – C. perfringens

• Occurs in severe traumaticwounds. – Contamination wi th dirt,

© DJ105

• Gunshot wounds• Gall bladder surgery.

– Rapidly life t hreatening• Can’t w ait for lab cultures.• Clinical diagnosis required.

– Detect gas in inf ected tissue.

Gas Gangrene Treatment• Remove infected tissue immediately.

– Surgical debridement – Place drain in w ound

© DJ106

Gas Gangrene Treatment

• Secondary treatments – Place patient in hyperbaric oxygen

© DJ107

c am er. – Treat with penicil lin.

Gas Gangrene Diagnosis• This is a clinical

diagnosis• Laboratory support

© DJ108

– Culture and Gram

stain – Tissue biopsy




MICR570/DJ/F12 24/25-28

Anaerobic Cellulitis• Clostridial infection of wounds and

surrounding subcutaneous tissue. – Marked gas formatio n. – Toxicity o f gas gangrene is absent.

© DJ109

• Less pain and swelling. – Other species of Clostridium plus other

anaerobes can cause this syndro me.

AnaerobicCellulitis

• Dog bite – Mixed anaerobi c

© DJ110

ora nc u ngClostridium

Non-Sporeforming Gram Posit ive Anaerobic Rods

• More pathogenic members – Actino myces – Propionibacterium

© DJ111

• Less pathogenic members – Mobiluncus (may help cause vaginiti s) – Lactobacillus

– Eubacterium – Rothia

Lactobacillus Colonies

• Resemble alphastreptococci – Normal vaginal flora.

© DJ112

– If Lactobacillus isreplaced withMobiluncus , vaginitisresults.




MICR570/DJ/F12 24/25-29

Actinomyces

• Long Gram pos itive rods –

© DJ113

• No spores, not acid fast

Common Actinomycetes

• A. i sr aeli i – Most common pathogen in serious

infection.

© DJ114

– “ Molar tooth” colony morphology. – Takes 4-10 days to g row .

• Other species – A. naeslun di i – A. meyer i

Act inomyces

• Can cause serious chroni c in fection. – Uterus with certain intrauterine devices – Aspi rat io n pneu monia

© DJ115

– Abscesses in neck or head• May see pus with granules in

infection. –

Called “ Sulphur Granules”• The granules are colonies of Actinomyces

Other Gram PositiveNon-Sporeforming Rods

• Propionibacterium species – Considered to be an anaerobe. – Normal skin flora

© DJ116

• ppor un s c pa ogen• Common blood culture contaminant.




MICR570/DJ/F12 24/25-30

Propionibacterium acnes

• Gram s tain:

© DJ117

Propionibacterium acnes

• Anaero bic “ coryneform”• Infections

– Acne

© DJ118

– of prost hetic devices.

– Part of mixed anaerobicinfections

Gram Negative Anaerobic Rods

• Bacteroides fragilis group – mostcommon Gram-negative rodscausing anaerobic infections. – 10 s eci es

© DJ119

• Penicill in resistant – B. fragilis is main member

• Capsule wi th antiphagocyticfunction.

• Fusobacterium sp. is #2.

Rickettsial Rashes

© DJ120




MICR570/DJ/F12 24/25-31

Characteristics of Rickettsia

• Gram-negative bacilli . – Strict intracellular

pathogens.

© DJ121

• Reservoir is in animals – Transmission often with

insect vector.• Diseases:

– Typically fevers with arash.

Insect Bite: Site of Transmiss ionof Rickettsial Infections

• Host is i nfectedby insect bite. –

© DJ122

infection,systemicinfectionfollows.

Rickettsial Pathogenesis

• Rickettsiae infect vascularendothelium.

© DJ123

– .• Result is rash & petechial lesions.• Same process occurs in o rgans.

– Causes systemic symptom s.

Rickettsia (RMSF) InvadeVascular Endothelium

• Cause of rashand hemorrhage – Ar row

© DJ124

indicatesstained areaof rickettsialorganisms incapillary




MICR570/DJ/F12 24/25-32

General ClinicalManifestations

• Rickettsial disease: – Fever and headache.

© DJ125

– External rash and int ernal focallesions.

– Endotoxin-like shock may occur.

Lab Diagnosis of RickettsialDisease: Look for Organism

• Culture is difficu lt and hazardous. – Culture is not widely available.

• Requires tissu e culture or eggs. – Don’t order this for routine testing.

© DJ126

• PCR is best. – Avai lab le i n l arger publi c health l abs .

• Enzyme immuno assays for antib odyprodu ction after infection are available. – OK for epidemiology and presumptive

diagnosis after the acute phase.

Review of Specific RickettsialDiseases Grouped by Vector

© DJ127

Tick: Dermacentor variabilis• Tick awaiting meal • Engorged tick

© DJ128




MICR570/DJ/F12 24/25-33

Rocky Mountain Spotted Fever(RMSF)

• Caused by Rickettsia rickettsii . – A simil ar d isease in rest of wor ld is

caused by R. conorii.

© DJ129

• sua y occurs n warmer mon s. – Most cases are in ch ild ren < 15 years. – History of ti ck bite is elicit ed in 70 % of

cases.

Clinical Manifestations of RMSF

• Incubation period after bite: 2-14 days – Fever, headache, confusion , myalgia.

• Rash is main characteristi c feature.

© DJ130

.• Appears on w ri sts and ankl es

– Trunk is also affected.• RASH ON PALMS AND SOLES is key

• Death in 25 % without t reatment.

Petichiae of Rocky Mountain SpottedFever

© DJ131

RMSF Day 9Note Facial Edemaand Rash

•

© DJ132

semi-coma – Note hemorrhage

around mouth.




MICR570/DJ/F12 24/25-34

Clinical Diagnosis of RMSF• This is a clinical diagnosis.

– If you see a compatibl e case historywith characteristic findings:

•

© DJ133

. – Diagnosis, even wi th PCR is too slow .

• Must send test to a reference lab.• Patient can’t w ait for treatment.

Therapy of RMSF

• Antibiot ic therapy is highly ef fec ti veduring fi rst week of ill ness. – Chloramphenicol is good for serious

<

© DJ134

. – Tetracycline is a second choice.

• Treatment r educes mort ality to 5-7%. – Most who die first got antibiotics

during second w eek of i llness.

Prevention of RMSF

• Av oid t ick con tac t. – Remove ticks w ithin 4-6 hours.

• They do not t ransmit d isease

© DJ135

sooner.• Killed vaccines are available for

military and for researchers – Not given to general publi c in USA.

Mite-Borne Rickettsia

• R. akari – Rickettsial pox

© DJ136

• . su sugamus – Scrub typhus




MICR570/DJ/F12 24/25-35

Rickettsialpox• Urban disease caused by R. akari .

– Transmitted by house mouse mite bite. – Found in New York City and poo rer

sections of o ther large cities in USA.

© DJ137

• Benign self-limiti ng illness. – Initial mite bite develops papul ovesicle. – Later, fever, follow ed by a rash. – Tetracyclin e is effective antibiotic. – Probably under diagnosed.

Rickettsial Pox Lesions: Initial Bite Site

• Early l esion • Older lesion - Eschar

© DJ138

Scrub Typhus• Caused by Rickettsia tsu tsugamushi.

– Disease of Asia and South Pacific.• Carried to man by rodent mites.

– Rodent mites remain infected forever by

© DJ139

transovarian transmission. – Lesion develops at initi al bite site.

• Symptoms like other typhus di seases

but mortality is low.

Pediculus humanus - Body Louse

• Vector for: – R. prowazekii

© DJ140

– B. quintana

• Trench fever




MICR570/DJ/F12 24/25-36

Louse-Borne Typhus Fever • Caused by Rickettsia prowazekii.

– Disease of w ar and upheaval.• Epidemics in refugees.• Louse control helps stop epidemics.

© DJ141

• Transmitted to man by body louse. – Louse becomes infected feeding on an

infected person. The louse will die of th einfection, but not before it feeds on ot hers.

• Louse defecates when it feeds. – Deposits organisms near bite wound.

Typhus Fever • Symptoms start 1-2 weeks after bit e.

– Fever, headache, malaise, myalg ia. – Rash on trunk, spreads to extremities. – Complications : CNS and h eart.

© DJ142

• Mortali ty 10-60 %.• Treatment and prevention:

– Tetracycline, chloramphenicol are OK. – Louse control stops epidemics.

Epidemic Typhus Fever Rash

• Rash seenafter 10

© DJ143

illness

Gangrene after Epidemic LouseBorne Typhus

• Compromisedcirculation.

© DJ144

– ue o n ec oninducedvascular injur y.




MICR570/DJ/F12 24/25-37

Recrudescent TyphusRickettsia prowazekii Relapse

• Synonym: B rill’ s Disease. – Relapse of lou se-borne typh us. – Occurs 10-40 years after first infection.

© DJ145

– • Rickettsiae remain dormant i n

reticuloendothelial cells.• Fading immu nity of ol d age allows

organism to attack again.

One Last Rash CausingBacterium to Mention

• Lyme disease

© DJ146

Borrelia burgdorferi

• A l arge spirochete 0.2 x 10-30 um. – Loose irregular spirals. – Stains weakly with ordi nary stains.

© DJ147 © DJ147

– u ure s cu• Not used clinically. For research only.

– Doubling time is long: 8-24 hours .•

Has t oxic lipopolysaccharide.

Epizoology of B. burgdorferi

• Transmitted to man by tick. – Ixodes carry infection throughout w orld.

• Ticks feed and mate on deer. – Female ticks deposit eggs on ground.

© DJ148 © DJ148

• Tick larvae infected by f eeding on white-footed mouse carrying B. burgdorferi .

– Larvae mature to nymphs and adult ticks• These feed on mous e and on man c ausing

infection in man.• Causes classic Lyme disease in man




MICR570/DJ/F12 24/25-38

Other Key Elements in Lyme DiseaseTransmission

• White footed deermouse

• Ixodes scapularis

© DJ149 © DJ149

Lyme Disease Dist ribu tion In USA

© DJ150 © DJ150

Clinical Manifestations of Lyme

• Several stages and rarely fatal: – Primary lesion.

• Erythema chronicum migrans.

© DJ151 © DJ151

– Secondary stage.• Spirochetemia + systemic symp toms.

– Late stage.•

Few organisms in diverse organs withimmun ologi cal mediated damage.

Primary Classic Lyme Disease

• Initial lesion – Occurs at ti ck b ite site 3-30 days later.

• Erythema chroni cum migrans (ECM). – Slowly expanding red ring.

© DJ152 © DJ152

– Biopsy of leading edge shows organism. – Disappear within weeks.

• Constitutional symptoms for months. – Fever, muscle and joint pains. – Meningeal irritation.




MICR570/DJ/F12 24/25-39

Small Nymph Stage ofTick In-situ With Early

Erythema Migrans

© DJ153 © DJ153

Early Lyme DiseaseErythema Chronicum Migrans - ECM

© DJ154 © DJ154

Borrelia burgdorferi Diagnosis• Organisms are present

in low numbers intissue. – Culture and stains are

© DJ155 © DJ155

. – Accep tab le tests:

• ElA for antibody plusWestern Bl ot.

• Rarely may use: – PCR of joint fluid .

Western Blo t Test forSpecifici ty of Antibody

to B. burgdorferi• EIA is better screening test

than the Western Blot. – Western Blot is helpful in

confirmation process of a Lyme

© DJ156 © DJ156

EIA screen as a follow up test.• Blot is MORE specific than

the EIA screening test. – Not all true infections wil l give

multipl e bands on the Westernblot assay, especially early inthe disease.

• May require a followupserum at a later date.




Prevention of Lyme Disease

• Avoid t ick b it es – Check for ticks and remove promptly.

• Insect repellent helps.• Wear lon ants tucked into socks.

© DJ157 © DJ157

• Light clothing helps to see ticks.

– Insecticide for ticks in infested lawns. – Remove rod ent habitat.

slides+for+posting+lecture+23+ +24+skin+blood+muscle+bacterial

Documents