A Case Study on RICHARD

Clinical
Group 5 GLYNN D.
Bacteriology Subgroup 1 ESTOMATA

JOMARIE EVE KURT RUSSEL ALVIN ROSTON

D. ENRIQUEZ A. JUMUAD R. PLATA

JESSA MAE C. JUDY ANN E. February

MENDOZA OMBROSA 26, 2011
 General Objective
To formulate specific, measurable,
attainable realistic and time
bounded differential diagnosis
toward the case to the patient.
Interpret laboratory results
accurately yet precisely.
Discuss the rationale of the
laboratory results to the clinical
diagnosis of the case patient.
Identify the etiology of the
disease of the patient.
Determine the immediate
preventive management care
of the patient’s case.
Explain well the salient anatomy
physiology and pathophysiology of the
case of the patient.
Know the action, mechanism, preparation
and side effects of the drugs, if there are
any, used by the patient prior to admission.
 PATIENT’S DATA AND HISTORY
PRE-EXAMINATION (after gastric bypass operation)
De Laune and Ladner (2006)

Objective
Subjective ● Inflammation of the
● Not available since patient’s membrane
there were no self- that lines the
reported symptom abdomen peritoneum
noted ● Surgical wound
infection
● Infection in the
connection of skin
and organs
 PHYSICAL EXAMINATION

Laboratory Examinations
General Appearance
Bacteriology
● A 45-year old female
accounted as a morbid obese
Culture and Sensitvity
or a body mass index greater
than 35 or 40-44.9. ● Isolation of Enteroccus species
Physical Tests from abdominal wound cultures
Not available ● Isolation of a strain of MRSA
with a linezolid minimal inhibitory
concentration (MIC) less than 4.
External Reference Laboratory (RITM, Alabang, Muntinlupa)
Culture and Sensitivity:

● Presence of MRSA having a linezolid resistance with a

MIC greater than 16

● Related organism resistant to cefazolin, ciprofloxacin,

chloramphenicol, clindamycin, erthromycin, gatifloxacin,
gentamicin, levofloxacin, oxacillin, and tetracycline but
susceptible to daptomycin, quinuprisitan-dalfopristin,
rifampin, trimethroprim-sulfamethoxazole and vancomycin

Reported Immediate Intervention Goals

● Administered IV vancomycin
 
 DEFFINITION OF THE CASE

INFECTIVE
ENDOCARDITIS 20 TO
SEPTICEMIA
 ANATOMY AND PHYSIOLOGY

CARDIOVASCULAR SYSTEM HEART

PATHOPHYSIOLOGY
Plate 1. Pre-pathophysiology Concept Map.
Plate 2. Pathophysiology Concept Map of a Possible Synergy of
Two Possible Strains
Plate 4. The ‘other side of the coin’ Pathophysiology.
 Fibrin-Platelet
Vegetation

Plate 3.The cycle presents the bottom line pathophysiology of the case of the
patient. Whether there is synergy of two strains of organisms or one organism
alone, the upshot is it follows the same common process above. The only
difference is their virulent factors present in each organism that may have
participated to the outcome of the disease.
Plate 4. The ‘other side of the coin’ pathophysiology
 ANTIBIOTIC OF INHIBITION ACTION
cefazolin R A first-generation cephalosporin antibiotic.
Their anti- bacterial activity is due to
inhibition of cell wall synthesis.

ciprofloxacin R A second-generation fluoroquinolone

antibacterial. It kills bacteria by interfering
with the enzymes that cause to rewind after
being copied, which stops synthesis of and
of protein.

chloramphenicol R Considered a prototypical

broad-spectrum antibiotic, alongside the
tetracyclines. a protein synthesis inhibitor,
inhibiting peptidyl transferase activity of the
bacterial ribosome.

clindamycin R It is a bacterial protein synthesis inhibitor by

inhibiting ribosomal translocation.
erythromycin R It interferes with the production of functionally
useful proteins, which is the basis of this
antimicrobial action.
gatifloxacin R An antibiotic of the fourth-generation
fluoroquinolone family, that like other members of
that family, inhibits the bacterial enzymes DNA
gyrase and topoisomerase IV.

gentamicin R An aminoglycoside antibiotic, used to treat many

types of bacterial infections, particularly those
caused by Gram-negative organisms.

levofloxacin R Levofloxacin is a broad-spectrum antibiotic that is

active against both Gram-positive and
Gram-negative bacteria. It functions by inhibiting
DNA gyrase, a type II topoisomerase, and
topoisomerase iv,[114] which is an enzyme necessary
to separate replicated DNA, thereby inhibiting cell
division.
 oxacillin R It is resistant to penicillinase enzymes, such
as that produced by Staphylococcus aureus,
it is widely used clinically in the US to treat
penicillin-resistant Staphylococcus aureus.

tetracycline R They inhibit protein synthesis by blocking

the attachment of charged aminoacyl-
tRNA. Thus they prevent introduction of
new amino acids to the nascent peptide
chain.
daptomycin S As a distinct mechanism of action,
disrupting multiple aspects of bacterial
cell membrane function. It appears to bind
to the membrane and cause rapid
depolarization, resulting in a loss of
membrane potential leading to inhibition
of protein, DNA and RNA synthesis, which
results in bacterial cell death.
quinuprisitan-dalfopristin S A combination of two antibiotics used to treat infections
by staphylococci and by vancomycin-resistant
Enterococcus faecium. Dalfopristin binds to the 23S
portion of the 50S ribosomal subunit, and changes the
conformation it, enhancing the binding of quinupristin[1]
by a factor of about 100. In addition, it inhibits peptidyl
transfer. Quinupristin binds to a nearby site on the 50S
ribosomal subunit and prevents elongation of the
polypeptide,[1] as well as causing incomplete chains to be
released.

rifampin S Rifampicin inhibits -dependent RNA polymerase in

bacterial cells by binding its beta-subunit, thus
preventing transcription to RNA and subsequent
translation to proteins.
trimethroprim- S Sulfamethoxazole inhibits bacterial synthesis of
sulfamethoxazole dihydrofolic acid by competing with para-aminobenzoic
acid (PABA). Trimethoprim inhibits enzymes of folic acid
pathways.
vancomycin S Vancomycin inhibits the second stage of cell wall
synthesis in susceptible bacteria. Furthermore, there is
evidence that vancomycin also alters the permeability of
the cell membrane and selectively inhibits ribonucleic
acid synthesis.

requires a
diagnostic strategy that is
both sensitive for disease
detection and specific for its
exclusion across all forms of
the disease
Summary
Moreover, signs and
thorough knowledge of the
symptoms of IE is at
anatomy and function of the
heart and the causes and constant, and this does not
contribute to the
effects of heart disease
continues to be a most differentiation of the strain
of organism causing the said
valuable tool illness
 Conclusion

Need for elimination is to be we should practice a The bottom point here is

scientific method of solving that the source of infection
drawn
a case study is nosocomial
 Recommendation

The diagnosis of IE is established (definite IE) if during a systemic infection involvement of

the endocardium is demonstrated.
 Recommendation

If, in addition, bacteraemia (positive blood cultures) or bacterial DNA are found, IE is
definite and culture/microbiologically positive, otherwise IE is definite but
culture/microbiologically negative.
 Recommendation

Criteria:
High Clinical suspicion
Prosthetic material inside heart
PCR
Peripheral abscess
First manifestation of CHF
Daghang Salamat