PI: 4 days prior to admission he complained of pain at his right
knee. He denied any history of trauma. He also felt "warm".
2 days prior to admission the fever persisted. Because of the pain he
could not walk. He was not given any other medication except paracetamol.
PH: He has been well until this illness.
VS: T 40 C, P 120/min, RR 32/min, BP 110/70 mmHg, body weight 43 kg (at 100 percentile)
GA: fully conscious
HEENT: with in normal range
LN: with in normal range
Heart: regular ,no murmur
Lung: clear
Abdomen: no organomegaly
Extremities: his right knee was in semi-flex position, mild swelling but marked tender of the the right thigh(just above the knee) figure 1
Skin : small pustular lesions at extrimities and face (figure 2)
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Figue 1
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Figure 2
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CBC : Hb 12.2 gm/dl, Hct 36.5%, WBC 12,200/cumm, N78% L7% M15%, Platelet 197,000/cumm
PBS: WBC: toxic granulation 1+ , no vacuolization, RBC: normochromic microcytic red cells,
E.S.R : 61 mm (at 60 min.)
U/A: with in normal range
CXR: with in normal range
Smear pustular lesion at the skin: see figure 3
X-rays of both legs: no abnormality seen
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Figue 3
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- The initial diagnosis of Staphylococcal septicemia was made and he was given intravascular cloxacillin (100 mg/kg/day).
- H/C 2/2 grew Staphylococus aureus.
- Fever persisted despite intravascular cloxacillin administration.
- On the 5th day of admission bone scan showed increased uptake at right femoral shaft with focally increased uptake at right epiphyseal region (figure 4) and the repeated E.S.R was 110 mm (at 60 min)
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Figue 4
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Surgical drainage obtained 30 cc. of pus (figure 5) under periostrium of the right femur. Pus smear: Gram positive coci in cluster (figure 6), but culture was no growth.
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Figue 5
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Figure 6
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The fever subsided in 24 hours after the surgical drainage (Figure 7). He was continued on intravenous cloxacillin. He finally was discharged home.
Final diagnosis: Acute osteomyelitis of right femur --> Staphylococcal septicemia
Suggested Reading: Chapter 183 Staphylococcus aureus. In : Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases, Fifth Edition. Written by Francis A. Waldvogel, M.D.
Staphylococci are among the hardiest non-spore-forming bacteria, and they can survive many nonphysiologic environmental conditions. They can be cultured from dried clinical material after several months, are relatively heat resistant, and can tolerate high salt media. Therefore, it is not surprising that despite the availability of potent antimicrobial agents, improved public health conditions, and hospital infection-control measures, Staphylococcus aureus has remained a major human pathogen. Indeed, the development of new antibiotic resistance and other epidemiologic conditions have reestablished this microorganism as a major pathogen in human diseases.
The natural history of S. aureus infections can be summarized as follows: many neonates and most children and adults will become intermittently colonized by S. aureus and harbor the organism either preferentially in their nasopharynx, occasionally on their skin and clothing, more rarely in the vagina (an important prerequisite in toxic shock syndrome [TSS]), or exceptionally in the rectum or perineal area. From these sites, S. aureus can contaminate any site on skin or mucous membranes or other subjects by interpersonal transfer, by aerosol, or by direct contact. The mucous membranes and the skin offer a very efficient mechanical barrier against local tissue invasion. If this barrier is breached by trauma or surgery, S. aureus may gain access to the underlying tissue and create a characteristic local abscess lesion that consists of necrotic tissue, fibrin, and a large number of live and dead polymorphonuclear leukocytes (PMNs). Toxin liberation to skin and other organs can cause various types of skin rash and general symptoms, as exemplified by TSS or acute diarrheal disease. At any time, multiplying bacteria can overcome local phagocytic mechanisms and gain access to the lymphatic channels and the blood stream. The ensuing staphylococcal bacteremia is a dreaded complication, and it can lead to metastatic infections (e.g., endocarditis, pneumonia, or osteomyelitis) and to the patient's demise. The many options of S. aureus to infect a patient are summarized in Table 183-1.
