Salmonella Microbiology Etiology Small gram-negative rods (2-4 X 0.5 microns) Most motile with flagella . Shigella and Klebsiella are non motile. facultative anaerobes. Reduce nitrate. Many genera: Escherichia, Salmonella, Shigella, Klebsiella, Proteus, Enterobacter, Yersinia, etc. Some strains are opportunistic pathogens. Some strains are true pathogens Salmonella, Shigella, Yersinia, some strains of E. coli. Enterobacteriaceae Etiology Etiology LPS on Surface Lipopolysaccharide Protective outer layer of most strains Memory immune response and antibodies directed against LPS Polymorphic nature of side chains is advantageous for bacteria Since Typhi has outer capsule, this infection is worse. Etiology Antigenic components of S. Typhi The O antigen (endotoksin, somatic antigen) Represent side chain of repeating oligosaccharide units projecting outwards from the LPS layer of the cell wall The H antigen (flagellar antigen) Occur in phase 1 and phase 2 The Vi antigen Located in outermost layer of S.typhi Outer membrane proteins (OMPs) Almost half of the mass of the outer membrane is protein (porin and non-porin proteins) Etiology Etiology Overview Typhoid fever, Salmonellosis, Typhus Enteric Fever Other Diarrhoeal diseases Paratyphoid Fever Non Typhoid Salmonella (NTS) S. Paratyphi A S. Paratyphi B / S. Schotsmuelleri S. Paratyphi C / S. Hirschfeldii Flea & Louse Borne Typhus Endemic Murine Typhus Epidemic Typhus Scrub Typhus Q Fever Rickettsia typhi Rickettsia prowazekii Orientia tsutsugamushi Typhoid Fever Salmonella typhi Salmonellosis Rickettsial Diseases Ehrlichioses & Anasplasmosis Tick & Mite Borne Fever Modes of Transmission Person to person transmition Rarely (bactery 10 - 10 6 ) Contamination of food products Salmonella live in the chicken intestine Contamination of food processing contamination of process equipment food presentation Affecting Factor 1. Microorganisms Factor -The number of ingested microorganisms -Serotypes and virulence strains
2. Host factors -Gastric acidity -Gastrointestinal motility -Normal flora -Humoral and cellular immunization system -Malnutrition -Metabolic and Nutritional Factors -Age -Other diseases -Use of antibiotics -Vaccinations -Duration of illness
3. Environmental Factors - Tropical and sub tropical - Urbanization - Standards of hygiene and sanitation SALMONELLOSIS Definition Salmonellosis is a common and widely distributed food-borne disease that is a global major public health problem affecting millions of individuals with significant mortality. Salmonellae live in the intestinal tracts of warm- and cold-blooded animals NonTyphoidal Salmonellosis ETIOLOGY : Salmonellae are motile, nonsporulating, nonencapsulated, gram-negative rods that grow aerobically and are capable of facultative anaerobic growth. They are resistant to many physical agents but can be killed by heating to 130F (54.4C) for 1 hr or 140F (60C) for 15 min. They remain viable at ambient or reduced temperatures for days and may survive for weeks in sewage, dried foodstuffs, pharmaceutical agents, and fecal material. Like other members of the family Enterobacteriaceae, Salmonella possesses somatic O antigens and flagellar H antigens. With the exception of a few serotypes that affect only 1 or a few animal species, such as S. dublin in cattle and S. choleraesuis in pigs, most serotypes have a broad host spectrum. Typically, such strains cause gastroenteritis that is often uncomplicated and does not need treatment, but can be severe in the young, the elderly, and patients with weakened immunity. The causes are typically S. Enteritidis (S. enterica serotype Enteritidis) and S. Typhimurium (S. enterica serotype Typhimurium), the 2 most important serotypes for salmonellosis transmitted from animals to humans
Host Factors and Conditions Predisposing to the Development of Systemic Disease with Non-typhoidal Salmonella Strains Neonates and young infants (3 mo of age) HIV/AIDS Other immune deficiencies and chronic granulomatous disease Immunosuppressive and corticosteroid therapy Malignancies, especially leukemia and lymphoma Hemolytic anemia, including sickle cell disease, malaria, and bartonellosis Collagen vascular disease Inflammatory bowel disease Achlorhydria or antacid medication use Impaired intestinal motility Schistosomiasis, malaria Malnutrition
Clinical Manifestation Acute Enteritis. The most common clinical presentation of salmonellosis is with acute enteritis. After an incubation period of 672 hr (mean, 24 hr), there is an abrupt onset of nausea, vomiting, and crampy abdominal pain, primarily in the periumbilical area and right lower quadrant, followed by mild to severe watery diarrhea and sometimes by diarrhea containing blood and mucus. A large proportion of children are febrile, although younger infants may exhibit a normal or subnormal temperature. Symptoms usually subside within 27 days in healthy children and fatalities are rare. However, some children develop severe disease with a septicemia-like picture (high fever, headache, drowsiness, confusion, meningismus, seizures, abdominal distention). The stool typically contains a moderate number of polymorphonuclear leukocytes and occult blood. Mild leukocytosis may be detected. Bacteremia. While bacteremia can occur with minimal associated symptoms in newborns and very young infants, in older infants it typically follows gastroenteritis and can be associated with fever, chills, and septic shock. In patients with AIDS, recurrent septicemia appears despite antibiotic therapy, often with a negative stool culture for Salmonella and sometimes with no identifiable focus of infection. Nontyphoidal Salmonella gastrointestinal infections commonly cause bacteremia in developing countries. High rates of invasive disease with S. Typhimurium and S. Enteritides reported from Africa (3870% of isolates) suggest an association with HIV infections and malaria. Extraintestinal Focal Infections. Following bacteremia, salmonellae have the propensity to seed and cause focal suppurative infection of many organs. The most common focal infections involve the skeletal system, meninges, and intravascular sites and sites of pre-existing abnormalities; areas of bone infarction as in sickle cell disease; or bone prostheses. Complication Salmonella gastroenteritis can be associated with acute dehydration and complications resulting from delayed presentation and inadequate treatment. Bacteremia in younger infants and immunocompromised individuals can have serious consequences and potentially fatal outcomes. Salmonella organisms can seed many organ systems, leading to intracranial infections (meningitis, focal brain abscesses) as well as osteomyelitis in children with sickle cell disease. Reactive arthritis may follow Salmonella gastroenteritis, usually in adolescents with HLA-B27 antigen. In certain high-risk groups, especially those with impaired immunity, the course of Salmonella gastroenteritis may be more complicated. Neonates, infants <6 mo of age, and children with primary or secondary immune deficiency may have symptoms persisting for several weeks. The course of illness and complications may also be affected by coexisting pathologies. In children with AIDS, the infection frequently becomes widespread and overwhelming, causing multisystem involvement, septic shock, and death. In patients with inflammatory bowel disease, especially active ulcerative colitis, Salmonella gastroenteritis may be potentially fatal, with rapid development of toxic megacolon, bacterial translocation, and sepsis. In children with schistosomiasis, the Salmonella may persist and multiply within schistosomes, leading to chronic infection unless the schistosomiasis is effectively treated. Prolonged or intermittent bacteremia is associated with low-grade fever, anorexia, weight loss, diaphoresis, and myalgias, and may occur in children with underlying problems and reticulo-endothelial system dysfunction such as hemolytic anemia or malaria.
Diagnosis Definitive diagnosis of Salmonella infection is based on clinical correlation of the presentation and culturing and subsequent identification of Salmonella organisms from feces or other body fluids. In children with gastroenteritis, cultures of stools have higher yields than rectal swabs. In children with nontyphoidal Salmonella gastroenteritis, prolonged fever lasting 5 days or more and young age should be recognized as risk factors closely associated with development of bacteremia. In patients with sites of local suppuration, aspirated specimens should be Gram stained and cultured. Salmonella organisms grow well on nonselective or enriched media, such as blood agar, chocolate agar, or nutrient broth, but stool specimens containing mixed bacterial flora require selective media such as MacConkey, xylose-lysine- deoxycholate (XLD), bismuth sulfite (BBL), or Salmonella-Shigella (SS) agar for isolation. Although other rapid diagnostic methods, such as latex agglutination and immunofluorescence, have been developed for rapid diagnosis of Salmonella in cultures, there are few comparable tests for rapid serologic detection. Polymerase chain reaction (PCR) techniques may offer a rapid alternative to classic cultures but are as yet not in widespread use in clinical settings
Identification of salmonella sp. ORGANISM AND INDICATION DOSE AND DURATION OF TREATMENT Salmonella infections in infants <3 mo of age, immunocompromised persons Cefotaxime 100200 mg/kg/day every 6 hr for 514 days or Ceftriaxone 75 mg/kg/day once daily for 7 days or Ampicillin 100 mg/kg/day every 6 hr for 7 days or Chloramphenicol 15 mg/kg/day divided every 6 hr PO for 510 days TABLE 195-3 -- Treatment of Salmonella Gastroenteritis Prognosis Most healthy children with Salmonella gastroenteritis recover fully. However, malnourished children and those who do not receive optimal supportive treatment (are at risk for developing prolonged diarrhea and complications. Y oung infants and immunocompromised patients often have systemic involvement, a prolonged course, and extraintestinal foci. In particular, children with HIV infection and Salmonella infections can have a florid course. After infection, nontyphoidal salmonellae are excreted in feces for a median of 5 wk. However, after clinical recovery from Salmonella gastroenteritis, asymptomatic fecal excretion of the organism may occur for several months, particularly in younger children or those treated with antibiotics. A prolonged carrier state after nontyphoidal salmonellosis is rare (<1%), but may be seen in children with biliary tract disease and cholelithiasis following chronic hemolysis. Prolonged carriage of Salmonella organisms is rare in healthy children but has been reported in those with underlying immune deficiency. During the period of Salmonella excretion, the individual may infect others, directly by the fecal-oral route or indirectly by contaminating foods. Typhoid Fever Definition of Typhoid Fever Acute enteric infectious disease caused by Salmonella typhi (S.Typhi). prolonged fever, Relative bradycardia, apathetic facial expressions, roseola, splenomegaly, hepatomegaly, leukopenia. intestinal perforation, intestinal hemorrhage ETIOLOGY Salmonella typhi Salmonella Paratyphi A Salmonella paratyphi B Salmonella chloreasuis ephidemiology Typhoid fever as an endemic disease in Indonesia In 1990 9,2 per 10,000 citizen In 1994 became 15,4 per 10,000 citizen 1981-1986 improved 35,8% : 19.596 26.606cases Epidemiology Fig. 1. The typhoid fever surveillance study sites http://www.who.int/bulletin/volumes/86/4/06-039818/en/ Incidence of typhoid fever Strongly endemic Endemic Sporadic cases Characteristic Typhoid fever PREVALENCE TYPOID FEVER Sign and symptoms Typhoid fever is characterized by a slowly progressive fever as high as 40 C (104 F), profuse sweating, gastroenteritis, and nonbloody diarrhea. Less commonly, a rash of flat, rose- colored spots may appear. In the first week : a slowly rising temperature with relative bradycardia Malaise headache and cough A bloody nose ( epistaxis) is seen in a quarter of cases abdominal pain is also possible leukopenia, with eosinopenia and relative lymphocytosis blood cultures are positive for Salmonella typhi or paratyphi The classic Widal test is negative in the first week.
Sign and symptoms In the second week of the infection : the patient lies prostrate with high fever in plateau around 40 C (104 F) bradycardia (sphygmothermic dissociation), classically with a dicrotic pulse wave Delirium is frequent, frequently calm, but sometimes agitated. This delirium gives to typhoid the nickname of "nervous fever Rose spots appear on the lower chest and abdomen in around a third of patients The abdomen is distended and painful in the right lower quadrant
There are rhonchi in lung bases Diarrhea can occur in this stage: six to eight stools in a day, green with a characteristic smell, comparable to pea soup constipation is also frequent The spleen and liver are enlarged (hepatosplenomegaly) and tender The Widal reaction is strongly positive with anti O and anti H antibodies Blood cultures are sometimes still positive at this stage. (The major symptom of this fever is the feve r usually rises in the afternoon up to the first and second week.)
Sign and symptoms In the third week of typhoid fever, a number of complications can occur: Intestinal hemorrhage due to bleeding in congested Peyer's patches; this can be very serious but is usually not fatal. Intestinal perforation in the distal ileum, this is a very serious complication and is frequently fatal. It may occur without alarming symptoms until septicemia or diffuse peritonitis sets in. Encephalitis Metastatic abscesses Cholecystitis Endocarditis osteitis
Sign and symptoms The fourth week : The fever has started reducing (defervescence stage) Fever come down, gradual improvement in all symptoms and signs, but still danger
The fifth week : convalescence stage disappearance of all symptoms, but can relapse Pathophysiology patogene Contaminated Food Stomach destroyed by HCl pass into the intestine reproduction Penetrate to epithelial cells (M cell) IgA <<< Lamina propria phagocyt by macrophages multiply in macrophages Peyeri plaque ileum distal Mesenterica lymph nodes Duct. thoracicus blood circulation Bakterimia 1 (asimptomatik) RES organ (hepar, spleen) left phagocytes Multiply in the extracellular organ/sinusoid blood circulation Bakterimia 2 (simptomatik) Hepar gall bladder intestinal lumen Faeces activated macrophages Hyperactive hyperplasia reaction plaque peyeri process continues erosion of blood vessels Necrotic hyperplasia penetrate the mucosa and muscle layer Perforation Release cytocin & infl rx penetrate the gut again delayed type hypersensitivity reaction Clinical forms Mild infection: very common seen recently symptom and signs mild good general condition temperature is 38 0 C short period of diseases recovery expected in 1~3 weeks young children mild more Clinical forms Persistent infection: diseases continue than 5 weeks Ambulatory infection: mild symptoms,early intestinal bleeding or perforation. Clinical forms Fulminate infection: rapid onset severe toxemia Septicemia High fever Chill circulation failure
Shock Delirium Coma Myocarditis bleeding Major findings in lower ileum Hyperplasia stage(1st week): swelling lymphoid tissue and proliferation of macrophages. Necrosis stage(2nd week): necrosis of swelling lymph nodes or solitary follicles. Ulceration stage(3rd week): shedding of necrosis tissue and formation of ulcer ----- intestinal hemorrhage, perforation . Stage of healing (from 4th week): healing of ulcer, no cicatrices and no contraction
Ink Mg I Mg II Mg III Mg IV Biakan Darah Biakan Feses Tes Widal Negatif Positif 60 90% Negatif Pos / Neg Negatif Positif 80 % Pos 50 % Negatif Positif 20 % Pos 50 % Pos 80 % MANIFESTASI KLINIK Diagnose LAB diagnose Rutine check -SGOT and SGPT increase -leukositosis (aneusinofilia and limfopenia) - LED increase WIDAL TEST Aglutination reaction between S. Typhii (antigen) with antibody (aglutinin) TUBEX test Detect antibody anti S.Typhi 09 in the serum of patient Typhidot TEST Antibody IGM and IG G in the outer membran of salmonela typhi IGM dipstick test Antibody IGM specific S.Typhii in the whole blood serum Blood culture Positive if typhoid fever but can be negative too Therapy Non farmaco Rest and therapy Diet farmaco DOSIS ES kloramfenikol 4x500 mg /Hari (oral/IV) Anemia aplastik tiamfenikol 4x500 mg/Hari Anemia aplastik klotrimoksazole 2x 2 tablet (sulfametoksazole 400 mg dan 80 mg trimetroprim) ampisilim 50-150 mg/KgBB sefalosporin 3-4 gram dalam dekstrosa 100 cc diberikan jam infus Complication Complication Intestinal -Bleeding intestinal -Perforation Non intestinal Hepatitis tifosa Pankreatitis tifosa Complication hematology Miokarditis neuropsikiatrik PREVENTION Choose food processed for safety Prepare food carefully Keep food contact surfaces clean Eat cooked food as soon as possible Maintain clean hands Steam or boil shellfish at least 10 minutes All milk and dairy products should be pasteurized Control fly populations Prevention of typhoid fever 1. Avoid risky foods and drinks. 2. Get vaccinated against typhoid fever. Remember that you will need to complete your vaccination at least 1 week before you travel so that the vaccine has time to take effect!! Taking antibiotics will not prevent typhoid fever; they only help treat it.
VACCINES Routine typhoid vaccination is indicated for: travelers to endemic areas, persons with intimate exposure to a documented S typhi carrier (e.g, household contact), and microbiology laboratory personnel who frequently work with S typhi
Vaccines are not approved for use children younger than 2 years.
Typhoid Vaccines Available in the United States Vaccine Name How Given Doses Total Time Needed to Set Aside For Vaccination Dosing interval Minimum Age Booster Needed Every... Ty21a 1 capsule per oral 4 2 weeks 2 days 6 years 5 years ViCPS 0.50 mL Intramuscular Injection 1 2 weeks Not applicable 2 years 2 years Treatment of complication 3. Toxic myocarditis: bed rest cardiac muscle protection drugs, dexamethasone, digoxin. Viral infection Such as upper respiratory tract infection. Abrupt onset with fever, headache, leucopenia, sore throat, cough, coryza. No rose spots, no enlargement of liver & spleen. The course of illness no more than 2 weeks. Differential diagnosis depends on typical manifestations and blood culture.
Malaria History of exposure to malaria. Paroxysms(often periodic) of sequential chill,high fever and sweating. Headache, anorexia, splenomegaly, anemia, leukopenia Characteristic parasites in erythrocytes,identified in thick or thin blood smears.
Dengue Fever Sudden high fever day 1-3 (above 38,5 o C), in day 3 or day 4-5 increase but not very high (below 38,5 o C) Typhoid fever enteritis Malaria Dengue fever Caused: Infection by Bacteria: Salmonella typhi, Salmonella paratyphi S. enteritidis bioserotypes (e.g., S. typhimurium)
Parasite: Plasmodium falciparum , P. vivax,P.ovale, and P.malariae 1 of the 4 serotypes of dengue virus, family Flaviviridae, genus Flavivirus incubation period 10-14 days
6-48hours 10 -15 days 4-7days symptomps Prolonged fever, headache, malaise and anorexia, constipation, bloody diarrhea Nausea, vomiting, nonbloody diarrhea, fever, cramps, myalgia and headache flu-like illness with fever, chills, muscle aches, and headache, nausea, vomiting,cough, and diarrhea. high fever, headaches, joint and muscle pain, vomiting and a rash, pain behind the eyes DIFFERENTIAL DIAGNOSIS Paratyphoids A, B & C The laboratory is usually required as the final authority. The paratyphoids tend to run a milder course with profuse rose spots. Salmonella infection and gastroenteritis Salmonellae, the dysentery group, and staphylococci may occasionally cause an invasive illness resembling typhoid fever with bacteremia. Usually, however, the gastrointestinal symptoms are more acute than the general manifestations, and the pyrexia much lower and of shorter duration.
DIFFERENTIAL DIAGNOSIS Other diseases in differential diagnosis a. Malaria This may be mistaken for typhoid in countries where both are endemic. A history of previous attacks, the more rapid onset in malaria, the shivering and sweating, the high early pyrexia, the relative infrequency of abdominal symptoms and signs, and a positive blood slide all point to a diagnosis of malaria.
b. Influenza Influenza may also be confused with typhoid, but is usually of much more rapid onset with high temperature, severe sore throat, cough, and the absence of a palpable spleen and rose spots.
DIFFERENTIAL DIAGNOSIS c. Bacillary dysentery This disease seldom causes much difficulty in diagnosis. The onset is usually acute, with severe blood diarrhoea, although in mild cases the blood may be absent. Diarrhoea with blood is rare in early typhoid. The signs and symptoms in dysentery are usually abdominal and remain so, the mental state and chest being clear.
d. Typhus and other rickettsial infections These conditions should be considered important when considering the differential diagnosis. This is because both typhus and typhoid can cause a febrile illness with delirium, chest signs, and abdominal discomfort. In typhus, however, the onset is acute, and the temperature high at an early stage. Shivering attacks are common at the onset, and prostration is rapid. The rash is quite different (brownish red in colour, and much more profuse). It does not fade on pressure, as does the rose spot in typhoid. There is a leucocytosis and the Weil-Felix test becomes significantly positive at about the tenth day.
Dengue Fever Dengue fever is virus based disease spread by mosquitoes. Most commonly the mosquito Aedes Aegypti. Sign and symptomp Criteria suspect of dengue fever Danger signs Character Dengue Fever Differential Diagnose Cause Dengue fever is caused by any one of four dengue viruses spread by the Aedes aegypti mosquito. DENGUE FEVER Symptoms High fever, up to 105 F (40.6 C) A rash over most of your body, which may subside after a couple of days and then reappear Severe headache, backache or both Pain behind your eyes Severe joint and muscle pain Nausea and vomiting DD - dengue fever Risk factors Young children and infants Travelers coming from areas with no malaria Pregnant women and their unborn children
MALARIA Symptoms Moderate to severe shaking chills High fever Profuse sweating as body temperature falls Headache Nausea Vomiting Diarrhea DD malaria Symptoms Fatigue Nausea and vomiting Abdominal pain or discomfort, especially in the area of your liver on your right side beneath your lower ribs Loss of appetite Low-grade fever Dark urine Muscle pain Itching Yellowing of the skin and eyes (jaundice) HEPATITIS A Differential diagnose Symptoms Abdominal pain Dark urine Joint pain Loss of appetite Nausea and vomiting Weakness and fatigue Yellowing of your skin and the whites of your eyes (jaundice)
HEPATITIS B Differential diagnose Symptoms Fatigue Fever Nausea or poor appetite Muscle and joint pains Tenderness in the area of your liver
HEPATITIS C Differential diagnose Caused by Salmonella paratyphoid A,B,C respectively. in no way different from typhoid fever in epidemiology, pathogenesis, pathology, clinical manifestations, diagnosis, treatment and Prophylaxis
PARATYPHOID FEVER A, B, C Differential diagnose Buku Ajar Infeksi & Pediatri Tropis ed.2, IDAI 2010 Harrisons Manual of Medicine 17 th ed, McGraw Hill Companies Inc. Disease Difference Hepatitis Low grade fever, dark urine, jaundice. Dx: AST & ALT level Dengue Fever Palatal vesicles, maculopapular rash, epistaxis, petechiae. Dx: blood - ELISA / PCR Brucellosis Febrile illness similar but less severe / fever & acute monarthritis @ hip or knee (septic arthritis) / long lasting fever & low back pain (vertebral osteomyelitis). Dx: Agglutination assays for IgM. Difficult to distinguish from TF & early symptom of TB TB Mostly confined in lung(s) with cough & purulent sputum production. GI TB peritonitis. Dx: peritoneal biopsy Malaria Febrile paroxysm at regular interval, (falcip) multiorgan dysfx. Dx: asexual form of parasites on peripheral blood smear Influenza Abrupt onset of systemic symptoms. Dx: tissue culture of virus from throat swab, nasopharyngeal wash, or sputum Tularemia (oropharyng & GI) Pharyngitis, cervical & mesenteric adenopathy, intestinal ulceration. Dx: microagglutination / tube agglutination test, PCR Gastroenteritis Diarrhea with stools containing blood, mucus, leukocytes. Dx: blood/stool cultures Bronchitis Bronchopneumonia Shigellosis w/o th/ most cases resolve in 1 week. Dx: stool culture Systemic fungal infections Incidence and Timing of Various Manifestations of Untreated Typhoid Fever Incubation Week 1 Week 2 Week 3 Week 4 Post Systemic Recovery phase or death (15% of untreated cases) 10%-20% relapse; 3%-4% chronic carriers; long-term neurologic sequelae (extremely rare); gallbladder cancer (RR=167; carriers) Stepladder fever pattern or insidious onset fever Very common Very common Acute high fever Very rare Chills Almost all Rigors Uncommon Anorexia Almost all Diaphoresis Very common Incubation Week 1 Week 2 Week 3 Week 4 Post Neurologic Malaise Almost all Almost all Typhoid state (common) Insomnia Very common Confusion/de lirium Common Very common Psychosis Very rare Common Catatonia Very rare Frontal headache (usually mild) Very common Meningeal signs Rare Rare Parkinsonism Very rare Ear, nose, and throat Coated tongue Very common Sore throat f
Incubation Week 1 Week 2 Week 3 Week 4 Post Pulmonary Mild cough Common Bronchitic cough Common Rales Common Pneumonia Rare (lobar) Rare Common (basal) Cardiovascular Dicrotic pulse Rare Common Myocarditis Rare Pericarditis Extremely rare g
Thrombophleb itis Very rare Incubation Week 1 Week 2 Week 3 Week 4 Post Gastrointestinal Constipation Very common Common Diarrhea Rare Common (pea soup) Bloating with tympany Very common (84%)
Diffuse mild abdominal pain Very common
Sharp right lower quadrant pain Rare
Gastrointestinal hemorrhage Very rare; usually trace Very common intestinal perforation Rare Hepatosplenome galy Common Jaundice Common Gallbladder pain Very rare Incubation Week 1 Week 2 Week 3 Week 4 Post Urogenital Urinary retention Common Hematuria Rare Renal pain Rare Musculoskeletal Myalgias Very rare Arthralgias Very rare Rheumatologic Arthritis (large joint) Extremely rare Dermatologic Rose spots Rare Miscellaneous Abscess (anywhere) Extremely rare Extremely rare Extremely rare prognosis Symptoms usually improve in 2 to 4 weeks with treatment. The outcome is likely to be good with early treatment, but becomes poor if complications develop. Symptoms may return if the treatment has not completely cured the infection.