Transcript ภาพนิ่ง 1

Case

A 23-year-old woman with a one-week
history of swelling and pain in her right
third finger was seen by an orthopedist,
who prescribed cephalexin and
indomethacin for suspected tenosynovitis.
Case

She presented to the emergency
department the day after pain developed
in her right ankle with generalized malaise.
PE showed a temperature of 39.4 C
and a rash.
What is your diagnosis?
What is further
management?
Presented by
Yaowapruek W.
18 Sep 2007
Introduction
Neisseria gonorrhoeae infects human
exclusively
 Colonize diverse mucosal surfaces ->
local and disseminated infections
 Most frequently reported communicable
disease in the US
 Most common cause of acute septic
arthritis in young sexually active adults

Contents
Epidemiology
 Pathogenesis
 Clinical features
 Differential diagnosis
 Culture
 Treatment

Annual incidence in US
Epidemiology
HIV epidemic -> reduction in number of
cases
 Peak incidence in men occurred at ages 20
-24, women at ages 15 – 19
 Disseminated gonococcal infection(DGI)
occurs between 0.5% and 3% of cases of
mucosal infection

Pathogenesis
Host Factors
Local mucosal-microbial
interaction
Complement activation
Cytokines
Women (perimenstrual
interval and pregnancy)
Microbial Factors
Pili
Protein IA
Protein II+
Protein III
Iron-repressible
membrane protein
Lipo-oligosaccharide
Proteoglycan
IgA proteases
Host factors
Male : female ratio = 1:4
 Gonorrhea in women often asymptomatic,
-> delayed treatment -> bacteria
spreading
 Pregnancy and perimenstrual interval
 Inherited complement deficiencies , esp
C5-C8 def

Surface of the Gonococcus
Microbial Factors
Mainly cell-surface structure
 Pili

 Major
virulence factor!
 Pili protein subunits, pili-associated proteins
 Two variations : antigenic, phase -> help
gonococci avoid host defense
Microbial Factors
Outer-membrane proteins
 Gonococci that lack of protein II in their
outer membrane may have an impaired
chemotactic response and are ass with
DGI.
 Protein IA and AHU (arginine,
hypoxantgine, uracil) strains more likely to
disseminate

Structure
Pathogenic Role
Pilus
Adherence to mucosa
Attachment to sperm
Inhibition to phagocytosis
Protein I
“Spiking” host cells
Protein II
Adherence to certain
mucosal cells
Adherence to neutrophils
Clumping of organisms
Structure
Pathogenic Role
Protein III
Binding site of blocking Ab
Lipopolysaccharide
Serum resistance
Toxic to ciliated fallopiantube cells (marked
endotoxic activity)
Peptidoglycan
Toxic to ciliated fallopiantube cells
Pathogenesis
Immune – mediated theory
 Aseptic inflammatory response

Clinical Features

Classic clinical triad in DGI
Dermatitis
DGI
Tenosynovitis
Migratory polyarthritis
Clinical Features

2 clinical pictures
Bacteremic infections (arthritis-dermatitis
syndrome) ~ 60%
 Localized septic arthritis ~ 40%

GU, Rectal,
Pharynx
Bacteremic
stage
Suppurative
arthritis
Patterns of arthritis
Migratory polyarthralgia
 Tenosynovitis
 Purulent arthritis

 Monoarthritis
 Polyarthritis

70%
67%
42 %
32 %
10 %
Diagnostic clue = Tenosynovitis ! and
pain often out of proportion with clinical
sign ( typically at hands and fingers)
Clinical Features
Joint involvement usu asymmetric,
involves knee, elbow, wrist, MCP, ankle.
 HIV -> unusual joint (hip,
sternoclavicular), aggressive course
 Synovial – WBC ~ 50,000 -200,000 and
PMN > 90%

Dermatitis
2/3 of cases
 Painless, nonpruritic skin rash ->usu. MP,
pustular, necrotic, or vesicular on an
erythematous base.
 Infrequently -> hemorrhagic skin lesions,
EN, urticaria, EM
 Occurs below the neck (body, limbs, palms
& soles) spare scalp, face and mouth

Dermatitis

Typically resolve over 4 to 5 days without
residual scarring
Rare manifestations
• Pericarditis, endocarditis esp aortic valve,
perihepatitis, pyomyositis, osteomyelitis,
meningitis
Differential diagnosis
Nongonococcal septic arthritis
 Reiter’s syndrome
 Rheumatic fever
 Syphilis
 Hepatitis and bacterial endocarditis

Lab tests
Mild leukocytosis
 Elevated ESR
 Mild anemia and abnormal LFT’s
 Gram stain

Culture
Positive C/S ->confirms the diagnosis and
allows determination of drug susceptibility
 Proven DGI = C/S from blood, synovial,
skin , other sterile sources
 Probable DGI = C/S from primary mucosal
sites
 Possible DGI = Typical clinical syndrome
and response to Rx without positive
culture

Culture
Site
Genitourinary
Synovial fluid
Rectum
Pharynx
Blood
Skin
Isolation rate (%)
80
25-50
20
10
5-10
Rare
Culture
Joint fluid and other sterile sites ->
Chocolate agar
 GU, rectum, pharynx -> Thayer-Martin
media
 Warmed c/s plate and plate specimens
bedside immediately

Treatment
Hospitalization is recommended if the
diagnosis is unclear, frank suppurative
arthritis, or poor compliance.
 Pts should be examined for clinical
evidence of endocarditis and meningitis
 Ceftriaxone 1 g iv OD is the mainstay
(Cefotaxime or ceftizoxime 1 g iv q 8 )

Treatment
Switched to a oral FQ after clinical
improvements for 24-48 hrs
(Ciprofloxacin, Levofloxacin)
 Treatment duration = 1 week
 Treat Chlamydia co-infection ->
doxycycline(100) 1*2 ~1 wk or single oral
dose of azithromycin (1g)

Treatment
Closed drainage of purulent effusions
 NSAIDs for alleviate pain and prevent
recurrent joint effusions
 Open drainage in difficult joints (i.e.hip)
 >1 episode of DGI -> work up for
complement deficiency!

Contents
Epidemiology
 Pathogenesis
 Clinical features
 Differential diagnosis
 Culture
 Treatment

Case

A complete blood count showed a
leukocyte count of 31,000 cells per cubic
millimeter. The patient reported having
had unprotected sexual intercourse during
the previous three weeks.
Case

A cervical culture was positive for
Neisseria gonorrhoeae

The patient’s symptoms and rash resolved
within three days after treatment
with intravenous ceftriaxone.