PATHOPHYSIOLOGY (BOOK-BASED)

Non-Modifiable Bacteria adhere and colonize Bacteria ascend to

perineum or the prepuce
Lower Urinary Tract Bacteria adhere and
Factors: urethra colonize bladder
Infection
 Female (shorter
urethra)
 Diabetic Bacteria adhere ureteral Cystitis
 Pathogens (E. mucosa and causes aperistalsis
Coli)
Modifiable Factors:
 Pregnant Woman Dilates ureter and flattens
 Nephrolithiasis renal papilla
 Vesicoureteral
Reflux (VUR)
 Catheterization
Pyelotubular backflow of
bacteria

Upper Urinary Tract Infection Adhesion of bacteria to

(“Pyelonephritis”) renal tubular cells

Inflammatory Response
Initiated Findings:
 (+) Bacterial Culture
 (+) Nitrite Test
 (+) Leukocyte Esterase
Release of
Test
Immunomodulators  Electrolyte
Abnormalities
 Palpable Lymph Nodes
Cytokines released
systematically

Activate Inflammation Spread to Systematic

locally Sites

Hypothalamus Medulla
Oblongata

Fever Nausea/ Vomiting

Dehydration Sunken Fontanel

 Urinary tract infections (UTIs) occur when bacteria, often originating from the fecal flora, migrate via
the urethra to the bladder causing symptomatic cystitis or asymptomatic bacteriuria. When an infection
occurs, lymph nodes in that area swell. Further ascension via the ureters leads to infection of the
normally sterile kidneys, termed pyelonephritis. The acute form of pyelonephritis is clinically defined as
a syndrome of bacteriuria with accompanied uni- and bi-lateral flank pain and tenderness, chills, and
sudden increase in temperature. It may encompass, or progress to, urosepsis, septic shock, and death.
Chronic pyelonephritis, on the other hand, is a radiological diagnosis defined by histological changes to
the renal tissue resulting from infection. Such changes may include renal scarring, fibrosis, tissue
destruction, and interstitial inflammation (Urinary Tract Infections: Molecular Pathogenesis and Clinical
Management, 2017).

A woman has a shorter urethra than a man does, which shortens the distance that bacteria must
travel to reach the bladder. Diabetics are three times more likely than non-diabetics to develop
pyelonephritis during a lower tract infection because of numerous factors. Pregnant women are also at
increased risk because of relaxation of smooth muscle around the ureters, which facilitates ascension of
infected urine from the lower tract as well as deficiencies in certain aspects of the normal immune
response. A woman has a shorter urethra than a man does, which shortens the distance that bacteria
must travel to reach the bladder. Patients with nephrolithiasis may have stones that become seeded
with bacteria, which make the bacteria very difficult to clear. Individuals with vesicoureteral reflux (VUR)
have multiple factors that render them susceptible to pyelonephritis. First, the retrograde flow of urine
from the bladder into the ureters facilitates bacterial ascension. Second, high-grade reflux into the
ureters during voiding can cause incomplete bladder emptying and urinary stasis. Third, chronic reflux
may cause upper tract scarring, which alters local antiadherence mechanisms. Fourth, those with reflux
are more likely to undergo catheterization and instrumentation, which promote colonization of the
urinary tract. Finally, lower tract infections may themselves increase the degree of reflux because of the
increased intracystic pressure associated with inflammation. Thus, individuals with vesicoureteral reflux
(VUR) often experience chronic pyelonephritis during childhood, which can lead to renal scarring if
severe and untreated. Several factors determine whether a given pathogen is likely to establish upper
tract infection. E. coli with type 1 and P fimbriae, for example, are more capable of adhering to the
urothelium, which facilitates ascension to the renal parenchyma. These mechanisms are particularly
important for pathogens causing pyelonephritis in anatomically normal urinary tracts. Bacteria are also
introduced into the bladder during catheterization of the urethra. Single catheterization of the bladder
in ambulatory patients results in a 1% incidence of subsequent UTI (The Netter Collection of Medical
Illustrations: Urinary System, 2012).

The initial events in acute pyelonephritis are most often due to P-fimbriae E. coli. By means of the tip
protein of P-fimbriae, the bacteria adhere and colonize the perineum or the prepuce, then ascend the
urethra. They adhere and colonize the bladder and in the case of the class III tip adhesin, cystitis may
occur. The E. coli may ascend the ureter if they contain the class II tip protein, adhere to the ureteral
mucosa, and cause aperistalsis. This dilates the ureter and flattens the renal papilla allowing
pyelotubular backflow of bacteria at a low pressure, thus allowing adhesion of bacteria to renal tubular
cells followed by invasive disease initiating pyelonephritis. As bacteria infect the upper tract, an
inflammatory response occurs (Urinary Tract Infection, 1997).

Upper tract infection is associated with a greater inflammatory response than lower tract infection,
and cytokines are increased in symptomatic infection as compared to asymptomatic infection.
 Symptomatic UTI—whether cystitis or pyelonephritis— represents an acute inflammatory response,
and the severity of infection reflects the magnitude of inflammation. Specifically, the outcome of
bacterial intrusion into the urinary tract appears to be determined primarily at the mucosal surface by
the innate immune response generated by the host. This response begins with specific interactions
between bacterial surface structures and epithelial cell receptors, leads to activation of host cell
signaling pathways and release of immunomodulators (including cytokines and chemokines), and results
in the recruitment of leukocytes.

Bacteria attach to the mucosal lining of the urinary tract and trigger a cytokine response. The cytokines
will in turn activate inflammation locally and spread to systemic sites where they cause fever and
nausea/vomiting (Diseases of the Kidney and the Urinary Tract : Diseases of the Kidney, 2006).

Urinalysis should be positive for leukocyte esterase, indicating the presence of white blood cells, and
nitrites, indicating the presence of bacteria. In some cases, serum chemistries may reveal azotemia or
electrolyte abnormalities secondary to dehydration. Urine culture and at least two sets of blood cultures
should be obtained before initiation of antibiotic therapy to determine if there is concurrent bacteremia
which show positive bacterial culture. Generally, as bacteria (The Netter Collection of Medical
Illustrations: Urinary System, 2012).
CLIENT-BASED

Non-Modifiable Bacteria adhere and colonize Bacteria ascend to

perineum or the prepuce
Lower Urinary Tract Bacteria adhere and
Factors: urethra colonize bladder
Infection
 Female (shorter
urethra)
 Pathogen (E.Coli) Irritant Dermatitis
Bacteria adhere ureteral Cystitis
Modifiable Factors: mucosa and causes aperistalsis
 Diarrhea
 Unhygienic
preparation of Dilates ureter and flattens
milk formula renal papilla
 Dirty surfaces
 Family having 5
stray cats
Pyelotubular backflow of
 bacteria

Upper Urinary Tract Infection Adhesion of bacteria to

(“Pyelonephritis”) renal tubular cells

Inflammatory Response
Initiated Findings:
 Colony Count: 100, 000
colonies/ml
 (+) Bacterial Culture [E.Coli]
Release of  (+) Nitrite Test
Immunomodulators  (+) Leukocyte Esterase Test
 Electrolyte Abnormality
o Day 1 (Sodium: 132;
Cytokines released Potassium: 3.4)
systematically  Anterior Lymph Nodes
Palpable

Activate Inflammation Spread to Systematic

locally Sites

Hypothalamus Medulla
Oblongata

Fever Nausea/ Vomiting

Dehydration Sunken Fontanel

Our patient is a 4-month old female and upon admission she showed sign of diarrhea. Being a female
means having shorter urethra is considered as a predisposing factor in which, having shorter urethra is
much easier for a bacterium to enter the body. And starting in precipitating factor is diarrhea in which it
is connected by the predisposing factor in which, fecal flora as one of the virulence factors that causes
pyelonephritis. Moving on the next precipitating factor, the unhygienic preparation of milk formula. As
the baby is fed by mixed breastfeeding and milk formula, unhygienic preparation of milk formula can be
the source of E. coli. In which, the baby bottle is unsterile, and the mother did not bother to change it,
she just directly used it to feed her baby. And, when preparing for the baby’s milk, the mother did not
wash her hands after doing something. Another precipitating factor is the dirty surfaces, when the
family have several areas in house in which has dirty surfaces and the baby is staying there frequently, it
increases the exposure of the baby to bacteria’s such as E. coli, adding that baby’s have the habit of
sucking their fingers. Lastly, as the family has 5 stray cats in their this can be another factor. As E. coli
can be found on both human and animals feces, once the baby or the mother unknowingly touched a
surface that has feces of those cats and the mother did not wash her hands before touching the baby,
specifically when touching the baby’s mouth, and when the baby sucked on her fingers, there is a
contact that can be a source E. coli. However, the closest possible factor that is present in our patient
that causes an infection are, patient having shorter urethra and diarrhea. As I have said earlier, an E. coli
is present in the feces of both human and animals, E. coli and fecal flora as one of the virulence factors
that causes pyelonephritis. Infection now starts when these bacteria migrate from the anus to
perivaginal area which adheres and colonize the perineum or the prepuce. This is evident by the irritant
dermatitis present in this area. Now, the bacteria ascend in the urethra causing the lower urinary tract
infection. Once the bacteria reached the bladder, it adheres and colonize in there, causing cystitis. The
bacteria now ascend in the ureters causing the bacteria to adhere ureteral mucosa which result to
aperistalsis. This dilates the ureter and flattens renal papilla which causes the pyelotubular backflow of
bacteria. Once the bacteria reached the kidney, adhesion of bacteria to renal tubular cells happen, and
this causes the upper urinary tract infection, or more commonly known as the pyelonephritis. As the
body detects an infection, it initiates an inflammatory response which now releases immunomodulators
(cytokines). In addition, once inflammatory response was initiated, the WBC now acts to fight infection,
making the lymph nodes in that area to be palpable. More so, cytokines are released systematically at
the site of infection or locally to initiate inflammatory response and to signal systematic sites such as
hypothalamus which causes fever ,and medulla oblongata which initiates nausea/vomiting. In addition,
nausea/vomiting causes dehydration as the body lose more fluids, in our patient, dehydration was
confirmed when physical assessment was done, where sunken fontanel was observed. Lastly, because of
nausea/ vomiting, the patient loses electrolytes which was evident on the laboratory findings under the
serum electrolyte test, the patient’s sodium and potassium levels were below the normal levels. The
findings that can be seen in the urine when urinalysis, and urine culture and sensitivity test was done are
presence of bacterial colony E. Coli, in which it counts 100, 000 colonies/ml, positive bacterial culture,
positive nitrite test which means that there is a presence of bacteria in urine, and positive leukocyte
esterase test which indicate the presence of UTI.

REFERENCES:

Bergan, T. (1997). Urinary Tract Infections (Vol. 1). Karger.

Kelly, C. R., & L., J. (2012). The Netter Collection of Medical Illustrations: Urinary System: Volume 5,

2e (2nd ed., Vol. 5). Saunders.

Nolte, F. S. (2017). Urinary Tract Infections: Molecular Pathogenesis and Clinical Management. ASM

Press.

Schrier, R. W. (2006). Diseases of the Kidney & Urinary Tract (Diseases of the Kidney (Schrier)) (8th

ed.). Lippincott Williams & Wilkins.