This hypothesis is supported by the isolation of from both the conjunctiva and oropharynx of documented BPF cases with H. aegyptius bacteremia. Possible virulence factors of H. aegyptius include lipooligosaccharides (LOS), capsular polysaccharides, pilus proteins (mediates adhesion to mucosal membrane), immunoglobulin A1 (IgA1), membrane associated proteins, and extracellular proteins. In a study conducted by Barbosa et al., a 60 kilodalton hemagglutinating extracellular product was suggested to be the major pathogenic factor linked to the hemorrhagic manifestations of BPF. This molecule was found to be absorbable by human O-type erythrocytes. After the molecule had been injected into rabbits, they showed reactions similar to that of BPF patients. Further research is being conducted to determine the mechanisms involved with the other virulence factors of H. aegyptius. The overall pathogenesis of BPF probably involves multiple steps and a number of bacterial factors. Diagnosis
A positive BPF diagnosis includes the clinical symptoms (mainly the fever, purpuric lesions, and rapid progression of the disease), isolation of Haemophilus Influenzae Biogroup aegyptius from blood, and negative laboratory tests for Neisseria meningitidis. The negative tests for Neisseria meningitidis rules out the possibility of the symptoms being caused by meningitis, since the clinical presentations of the two diseases are similar. Prevention
The basic method for control of the conjunctivitis includes proper hygiene and care for the affected eye. If the conjunctivitis is found to be caused by H. aegyptius Biogroup III then prompt antibiotic treatment preferably with rifampin has been shown to prevent progression to BPF.
Vesicoureteral reflux (VUR), also known as vesicoureteric reflux, is a condition in which urine flows retrograde, or backward, from the bladder into one or both ureters and then to the renal calyx or kidneys. Urine normally travels in one direction (forward, or anterograde) from the kidneys to the bladder via the ureters, with a 1-way valve at the vesicoureteral (ureteral-bladder) junction preventing backflow. The valve is formed by oblique tunneling of the distal ureter through the wall of the bladder, creating a short length of ureter (1–2 cm) that can be compressed as the bladder fills. Reflux occurs if the ureter enters the bladder without sufficient tunneling, i.e., too "end-on". Signs and symptoms
Most children with vesicoureteral reflux are asymptomatic. Vesicoureteral reflux may be diagnosed as a result of further evaluation of dilation of the kidney or ureters draining urine from the kidney while in utero as well as when a sibling has VUR (though routine testing in either circumstance is controversial). Reflux also increases risk of acute bladder and kidney infections, so testing for reflux may be performed after a child has one or more infections. In infants, the signs and symptoms of a urinary tract infection may include only fever and lethargy, with poor appetite and sometimes foul-smelling urine, while older children typically present with discomfort or pain with urination and frequent urination. Causes
In healthy individuals the ureters enter the urinary bladder obliquely and run submucosally for some distance. This, in addition to the ureters muscular attachments, helps secure and support them posteriorly.