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Toxic Shock Syndrome due to aureus pyelonephritis in diabetic

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					    Pyelonephritis due to
S. aureus: an unusual case of
   Toxic Shock Syndrome.

                     Maureen Shevlin Gutierrez, MD
             Georgetown University Internal Medicine
                                   Washington, D.C.
                                       May 13, 2006
Toxic Shock Syndrome (TSS)
 A rare but life-threatening bacterial illness.
 Caused by Staphylococcus aureus or by Group A
  Streptococcus bacteria.
 Historically, TSS has been a well recognized entity in
  menstruating females using tampons.
 More recently, TSS has been associated with surgical
  cases, skin and soft tissue infections, and postpartum
  complications.
 TSS requires early diagnosis and treatment as the case-
  fatality ratio is approximately 3% in menstrual cases,
  and 5% in nonmenstrual cases.
  How is the diagnosis made?
 TSS is a clinical diagnosis with 6 criteria:

     1.   Fever
     2.   Hypotension
     3.   Rash
     4.   Desquamation (1-2 weeks after illness onset)
     5.   Abnormalities in 3 or more organ systems
     6.   Negative blood, throat, CSF cultures
          - Blood cultures may be + for S. aureus (5% of cases)
          - 80-90% have S. aureus isolated from wound, or nasal cultures


 Definite cases fulfill 6/6 criteria, probable cases 5/6.
Case Presentation
                        HPI
 A 33 yo female with a history of DM2 presented to her
  PCP complaining of dysuria, urgency, and frequency.
  She denied fevers, chills, or back pain. She was
  diagnosed with a UTI and given a prescription for
  Macrobid. She returned to her physician 7 days later
  with persistent dysuria and back pain. She mentioned
  she had developed an erythematous rash. She was told
  to stop the Macrobid, and was given instead a
  prescription for Ciprofloxacin.
               HPI continued
 She presented to the emergency room 2 days later with
  worsening symptoms, fever, and an erythematous rash
  on her upper extremity extensor surfaces, as well as her
  lower extremities. After a CT scan of her chest,
  abdomen, and pelvis was completed, the patient became
  asystolic. She was coded three times, intubated, and
  placed on pressor support.
               Physical Exam
 T 102     BP 90/50 (on Levophed)     HR 120
  Assist Control respiratory support
 Perrla, mmm without mucosal lesions
 Tachycardic, no murmur appreciated
 Lungs with coarse breath sounds
 Abdomen soft, nondistended, BS+
 No menstruation
 Extremities without cyanosis, clubbing or edema
 Skin: Small bullae present on forearm extensor surfaces,
  erythematous lower extremity rash (that later became
  bullous), and a hemorrhagic lesion on her left thenar
  surface.
                   Laboratories
  124     88       153
                         506
  4.6     13       6.1
                                         12.2
       4     1.1                 31.4             254
     1.4     0.6                        35.8
     113     52                90N/ 5 Bands/ 3L
         169

CPK 936                  Blood Culture: No Growth
Lactic acid 5.9          Urine Culture: MSSA
                     Imaging
 CHEST CT: Multiple solid and cavitary nodules
  representing septic emboli. Bibasilar consolidations.

 ABD CT: Bilateral nephrolithiasis with obstructing left
  UPJ calculus. Left ureteral dilation and enlarged left
  kidney with associated inflammatory changes. No
  foreign bodies (no tampons, IUD, or contraceptive
  sponge.)

 MRI: Marked left pyelonephritis with innumerable areas
  of nonenhancement representing infarction or abcess.

 ECHO (TEE): No vegetations.
               The diagnosis
 Our patient met 6/6 criteria for TSS:
   • T 102
   • BP requiring pressor support
   • Erythematous and bullous rash
   • Cardiac, respiratory, and renal failure.
   • Her blood cultures remained negative. Both her urine
     culture, as well as culture of fluid from a nephrostomy
     tube placed shortly after admission, grew MSSA.
   • Her skin desquamated approximately one week after
     admission.
   Staphylococcal
Toxic Shock Syndrome
          Staphylococcal TSS
 1920 to 1979: Fever, hypotension, and multi-organ
  failure in young women is described.
 1978: TSS with S. aureus is described in pediatric cases.
 1979 to 1980: The epidemic years
   • 1980: 812 cases of menses-related TSS
                                  MMWR Morb Mortal Wkly Report 1983; 32: 398

 1981 to 1986: Increase in awareness
 1986: Active surveillance
 1987 to 1996: Surveillance and precautions

 Between 2002 and 2003, the number of cases reported
  to the CDC rose by 18%.
            The years 1979 to 1996
   5,296 cases were dx, 74% assc with menstruation
   93% of total cases occurred in women
   73% of nonmenstrual cases occurred in women.
   An increase in awareness, surveillance, as well as
    precautions, led to a decrease in the incidence:
     •    9 / 100,000 women in 1980
     •    1 / 100,000 women in 1986
                                                                  MMWR Morb Mortal Wkly Report 1990; 39: 421

 The % of cases associated with menstruation also
  decreased:
     • 91% during 1979-1980 to
     • 71% during 1981-1986 to
     • 59% during 1987-1996



Hajjeh RA, Reingold A, Weil A, et al. Toxic shock syndrome in the United States: surveillance update, 1979 -1996. Emerg
Infect Dis J. 1999;5:no. 6.
  Menstrual vs. Nonmenstrual




Reingold AL, et al. Toxic shock syndrome surveillance in the United States, 1980 to 1981. Ann Intern
Medicine 1982;96 (part 2):875-80.
        Nonmenstrual cases
41% of the cases of TSS that occurred between the
years 1987-1996 were nonmenstrual.
             Nonmenstrual Cases
 A review of 130 cases (in 1982) by Reingold et al
  revealed the three previously mentioned TSS
  associations, as well as adenitis, bursitis, abscesses, and
  bacteremia as etiologies.
 73 percent of nonmenstrual cases were in women.
  However, the distribution between genders was equal if
  vaginal and postpartum-associated cases were excluded
  in one study.
 The proportion of cases following surgical procedures
  increased from 14% in 1979-1986 to 27% in 1987-1996.
 Other documented cases: mastitis, sinusitis,
  osteomyelitis and arthritis, burns, and respiratory
  infections following influenza.
Reingold AL; Dan BB; Shands KN; Broome CV. Toxic-shock syndrome not associated with menstruation. A
review of 54 cases. Lancet 1982 Jan 2;1(8262):1-4.
                      Literature search
 Kivota et al described MRSA TSS in a patient with
  chronic complicated pyelonephritis after endopyelotomy
  for hydronephrosis.




  Kivota, H; Ohishi Y, et al. Correlation in Staphylococcus aureus infections between toxic shock syndrome toxin -1
  production and clinical feature. Kansenshogaku Zasshi. 1998 Jun;72(6):593-8.
                     Case fatality ratio
 The case-fatality rate                         5% Nonmenstrual (this rate
  has declined for                                has not decreased over time)
  menstrual TSS from                                  • Occurs in less healthy
                                                      • Diagnostic biases
     • 5.5% in 1979-1980 to
                                                      • Reporting biases (underreporting
     • 2.8% in 1981-1986 and                            common)
     • 1.8% in 1987-1996                              • Late treatment




Hajjeh RA et al. Toxic shock syndrome in the United States: surveillance update, 1979-1996. Emerg
Infect Dis J. 1999;5:no. 6.
          Why is it so virulent?
 S. aureus toxins
   • Toxic shock syndrome toxin 1 (TSST-1)
         90-100% of isolates producing menstrual cases TSS
         40-60% of isolates assc. with nonmenstrual cases
    Enterotoxins A, B, C, D
      • Enterotoxin A (May be a virulent cofactor)
      • Enterotoxin B
           38-62% nonmenstrual, TSST-1 negative strains
      • Enterotoxin D
           Higher incidence in patients with S. aureus isolated in
            blood cultures.
Virulence = Superantigens
                             Treatment of TSS
 Nafcillin to treat S. aureus infection
       • PCN has its best effect in the early stages of infection as it works by
         binding with PCN-binding proteins. PCN-binding proteins are lost during
         stationary-phase growth in vitro.
 Clindamycin to suppress protein (and thereby toxin and
  TNF alpha) synthesis.
 IVIG is controversial
       • Darenburg et al noted that culture supernatants containing superantigen
         from S. aureus were less efficiently inhibited by IVIG than those from S.
            pyogenes.
       • In the largest Streptococcal TSS series 21 patients were given IVIG and
         compared to 31 historical controls. Mortality was decreased from 66% to
         33%. However, fewer control patients were treated with Clindamycin.

Stevens, DL, Yan, S Bryant, AE. Penicillin binding protein expression at different growth stages determines penicillin effica cy in vitro and vivo: An
explanation for the inoculum effect. J Infect Dis 1993; 167:1401
Darenberg J; Soderquist B. Differences in potency of intravenous polyspecific immunoglobulin G against streptococcal and staphylococcal
superantigens: implications for therapy of toxic shock syndrome. Clin Infect Dis 2004 Mar 15;38(6):836-42. Epub 2004 Mar 1.
Kaul, R, McGeer, A, Norrby-Teglund, A, et al. Intravenous immunoglobin therapy for streptococcal toxic shock syndrome A compara tive
observational study. Clin Infect Dis 1999; 28:800
              Patient Update
 Our patient was treated with a nephrostomy tube,
  Nafcillin and Clindamycin, and also received 5 days of
  IVIG.
 She did well, and was discharged after four months of a
  complicated hospitalization.
            Take home points
 Toxic shock is no longer predominately a disease of
  menstruating females.
 Almost 50% of cases are nonmenstrual, which include
  post-surgical procedures, skin and soft tissue infections,
  and postpartum complications.
 Our literature search revealed that “unusual sites” have
  previously been reported.
 Our case, along with one other previously reported case,
  demonstrates that pyelonephritis should be added to this
  growing list of unusual sites of infection associated with
  S. aureus TSS.
 Recognition of the syndrome despite the site of infection
  is crucial to diagnosis and management.

                                           Resources
    Hajjeh RA, Reingold A, Weil A, et al. Toxic shock syndrome in the United States: surveillance update, 1979-1996. Emerg
    Infect Dis J. 1999;5:no. 6.
   Reingold AL, Hargrett NT, Shands KN, Dan BB, Schmid GP, Strickland BY, et al. Toxic shock syndrome surveillance in the
    United States, 1980-1981. Ann Intern Med 1982;96 (part 2):875-80.
   Update: toxic-shock syndrome– United States. MMWR Morb Mortal Wkly Report 1983; 32: 398
   CDC: Case definitions for public health surveillance. MMWR Morb Mortal Weekly Rep 1990; 39(RR-3):1
   Reduced incidence of menstrual toxic-shock syndrome: United States 1980-1990. Morb Mortal Wkly Rep 1990; 39:421.
   Jeffrey Parsonnet, Melanie A. Hansmann, Prevalence of Toxic Shock Syndrome Journal of Clinical Microbiology, September
    2005, p. 4628-4634, Vol. 43, No. 9
   H Reingold, AL, Dan, BB, Shands, KN, Broome, CV. Toxic shock syndrome not associated with menstruation. A review of
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   Ferguson, MA, Todd, JK. Toxic shock syndrome associated with Staphylococcus aureus sinusitis in children. J Infect Dis
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   Morrison, VA, Oldfield EC, 3rd . Postoperative toxic shock syndrome. Arch Surg 1983; 118:791
   Paterson, MP, Hoffman EB, Roux, P. Severe disseminated staphylococcal disease associated with osteitis and septic arthritis.
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   Reingold AL, Hargrett NT, Dan BB, et al. Nonmenstrual toxic shock syndrome: a review of 130 cases. Ann Intern Med 1982;
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   Reingold AL; Dan BB; Shands KN; Broome CV. Toxic-shock syndrome not associated with menstruation. A review of 54
    cases. Lancet 1982 Jan 2;1(8262):1-4.
   Schlievert, PM. Staphylococcal enterotoxin B and toxic-shock syndrome toxin-1 are significantly associated with non-
    menstrual TSS. Lancet 1986; 1:1149
   Lee, VT, Chang, AH, Chow, AW. Detection of staphylococcal enterotoxin B among toxic shock syndrome (TSS) and non-
    TSS- associated Staphylococcus aureus isolates. J Infect Dis 1992; 166:911
   http://student.ccbcmd.edu/courses/bio141
   Stevens, DL, Yan, S Bryant, AE. Penicillin binding protein expression at different growth stages determines penicillin effica cy
    in vitro and vivo: An explanation for the inoculum effect. J Infect Dis 1993; 167:1401
   Darenberg J; Soderquist B. Differences in potency of intravenous polyspecific immunoglobulin G against streptococcal and
    staphylococcal superantigens: implications for therapy of toxic shock syndrome. Clin Infect Dis 2004 Mar 15;38(6):836-42.
    Epub 2004 Mar 1.
   Kaul, R, McGeer, A, Norrby-Teglund, A, et al. Intravenous immunoglobin therapy for streptococcal toxic shock syndrome A
    comparative observational study. Clin Infect Dis 1999; 28:800
   Todd, JK, Ressman, M, Caston, SA, et al. Corticosteroid therapy for patients with toxic shock syndrome. JAMA 1984;
    252:3399

				
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