In the United States it is estimated that children 5 years and younger are the most at risk, receiving 50% of the total exposure, followed by laboratory personnel and then pet store employees. Other groups at increased risk are people over 65 years old, immunocompromised individuals, and pregnant women.Symptoms of RBF include sudden high temperature fevers with rigors, vomiting, headaches, painful joints/arthritis. A red, bumpy rash develops in about 75% of subjects. Symptoms of RBF can develop between 3 days and 3 weeks after exposure. While symptoms differ between Streptobacillary and Spirillary RBF, both types exhibit an incubation period before symptoms manifest. Due to its symptoms, RBF is often misdiagnosed by clinicians, leading to lingering symptoms and worsening conditions in patients; left untreated the mortality rate (death rate) of RBF is 13%. Even when treated, RBF can lead to migratory polyarthralgia, persistent rash, and fatigue  which can persist for weeks to years after initial infection and treatment. See also
Pasteurellosis
List of cutaneous conditions
Zoonosis

References
Rat Bite Fever (RBF) | CDC

Further reading
"Rat-bite Fever (RBF)". Centers for Disease Control and Prevention. Retrieved 28 February 2014. Centers for Disease Control Prevention (CDC) (January 2005). "Fatal rat-bite fever—Florida and Washington, 2003". MMWR Morb. Mortal. Wkly. Rep. 53 (51): 1198–202. PMID 15635289. Rat-bite fever (MyOptumHealth.com)
Tandon, R; Lee, M; Curran, E; Demierre, MF; Sulis, CA (Dec 15, 2006). "A 26-year-old woman with a rash on her extremities". Clinical Infectious Diseases. 43 (12): 1585–6, 1616–7. doi:10.1086/509574. PMID 17109293. Centers for Disease Control, (CDC) (Jun 8, 1984). "Rat-bite fever in a college student--California". MMWR.
Radiological abnormalities include things such as: trabeculated bladder, vesicoureteral reflex, external sphincter spasm, pyelonephritis, hyperreflexic bladder, noninhibited detrusor contraction, etc. Urinary abnormalities might result in renal deterioration and failure. This can be prevented by taking proper measures to restore normal micturition and by taking antibiotics to prevent infections. In some cases, the affected patients become hypertensive and progress to end-stage renal disease, while others become uremic. Additionally, most patients suffer from constipation. Early detection of this syndrome is possible through the peculiar faces that children present. Cause
Urofacial syndrome occurs due to either disruption or mutation of a gene on chromosome 10q23q24. The gene is located on a 1 centimorgan interval between D10S1433 and D10S603. Alteration of this gene leads to alteration of facial and urinary developmental fields. This gene is believed to be the HPSE2 gene. The HPSE2 gene is expressed in both the central nervous system as well as the bladder. Heparanase 2 is protein coded by exons 8 and 9 on the HPSE2 gene. This protein is believed to be altered in the case of this syndrome. Studies performed on mice indicate that HPSE2 has no enzymatic activity.Mutations in the HPSE2 gene on chromosome 10q23q24 have been observed to cause Ochoa Syndrome. This means the defective gene responsible for the disorder is located on an autosome (chromosome 10 is an autosome), and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder.