Could somebody tell me the scientific explnation of fever due to having a pyelonephritis?

One model for the mechanism of fever caused by exogenous pyrogens includes lipopolysaccharide (LPS), which is a cell wall component of gram-negative bacteria commonly seen in pyelonephritis. An immunological protein called Lipopolysaccharide-Binding Protein (LBP) binds to LPS. The LBP-LPS complex then binds to the CD14 receptor of a nearby macrophage. This binding results in the synthesis and release of various endogenous cytokine factors, such as interleukin 1 (IL-1), interleukin 6 (IL-6), and the tumor necrosis factor-alpha. In other words, exogenous factors cause release of endogenous factors, which, in turn, activate the arachidonic acid pathway.


PGE2 release
PGE2 release comes from the arachidonic acid pathway. This pathway (as it relates to fever), is mediated by the enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), and prostaglandin E2 synthase. These enzymes ultimately mediate the synthesis and release of PGE2.

PGE2 is the ultimate mediator of the febrile response. The set-point temperature of the body will remain elevated until PGE2 is no longer present. PGE2 acts near the ventromedial preoptic area (VMPO) of the anterior hypothalamus and the parvocellular portion of the periventricular nucleus (PVN), where the thermal properties of fever emerge. It is presumed that the elevation in thermoregulatory set-point is mediated by the VMPO, whereas the neuroendocrine effects of fever are mediated by the PVN, pituitary gland, and various endocrine organs.


Hypothalamus response
The brain ultimately orchestrates heat effector mechanisms. These may be

increased heat production by increased muscle tone, shivering and hormones like epinephrine.
prevention of heat loss, such as vasoconstriction.
The autonomic nervous system may also activate brown adipose tissue to produce heat (=non-exercise associated thermogenesis, also known as non-shivering thermogenesis), but this seems mostly important for babies. Increased heart rate and vasoconstriction contribute to increased blood pressure in fever.

The pathophysiology of UTI reflects a complex interaction between virulence factors of the microorganisms and the host defense.[9] The perineal flora are normal inhabitants of the distal urethra. Urine in the proximal urethra, the urinary bladder, and more proximal sites within the urinary tract is normally sterile. Uropathogens must gain access to the urinary bladder and proliferate if infection is to occur. Bacteria in the distal urethra may gain access to the bladder because of turbulent urine flow during normal voiding, as a consequence of voiding dysfunction, or as a result of the use of instrumentation. In any case, normal voiding results in essentially complete washout of contaminating bacteria. Therefore, urinary bladder colonization does not usually occur unless bladder defense mechanisms are impaired or a virulent strain of bacteria has gained access to the bladder.

In the absence of normal bladder emptying, there is proliferation of bacteria in bladder urine and the risk of a UTI. Even with normal bladder emptying, adherence to uroepithelial cells by virulent organisms such as P-fimbriated Escherichia coli may result in a UTI. P fimbriae (or pili) are organelles on E coli that mediate attachment to specific receptors on uroepithelial cells and impair washout of the bacteria.[10] The majority of UTIs in neurologically and anatomically intact children are caused by E coli. Children with intestinal carriage of P-fimbriated E coli are at increased risk for UTI because of colonization of the periurethral area by these pathogens.[11]