SALMONELLOSIS

Condes Dela Cruz Zapata

 Genus SALMONELLA Highly adapted for growth in both humans and animals. S. typhi and S. paratyphi restricted to human hosts ENTERIC or TYPHOID FEVER. Other serotypes NONTYPHOIDAL SALMONELLA.

ETIOLOGY
Salmonella are classified based on: 1. Somatic O antigen 2. Surface Vi antigen 3. Flagellar H antigen Most laboratories perform simple agglutination reaction that define spcific O antigen serogroups.

PATHOGENESIS
MOT: Ingestion of organism. Infectious dose: 10 3 10 6 CFU. Factor that increase susceptibility: 1. Decrease stomach acidity or intestinal integrity 2. Alteration of intestinal flora Type 3 secretion system

TYPHOID FEVER
Systemic infection Salmonella enterica serotype Typhi (S. Ty-phi) and S. enterica serotpe Paratyphi (S. Paratyphi) A, B, and C. Causes of febrile illness in crowded and impoverished populations with inadequate sanitation that are exposed to unsafe water and food and also pose a risk to travelers visiting countries of endemicity.
http://cid.oxfordjournals.org/cont ent/50/2/241.full

TYPHOID FEVER
An estimated 22 million cases of typhoid fever and 200,000 related deaths occur worldwide each year 6 million cases of paratyphoid fever are estimated to occur annually. Most of cases are in recent travelers. The risk of typhoid fever is highest for travelers to southern Asia

TYPHOID FEVER
The majority of cases in endemic countries are due to S. typhi. S. paratyphi is more common among travelers, perhaps because travelers tend to be vaccinated against S. typhi (there are no effective S. paratyphi vaccines). In endemic areas children and adolescents are affected most often.

TYPHOID FEVER
Foodborne and waterborne High incidence correlates 1. Poor sanitation 2. lack of access to clean drinking water Incubation period: 10 14 day depend on inoculum size and host health and immune system.

TYPHOID FEVER
CLINICAL COURSE Fever and abdominal pain hallmark of the disease but variable S. typhi: Prolonged Fever S. paratyphi: Gastrointestinal symptoms High index of suspicion

TYPHOID FEVER
CLINICAL COURSE Insidious onset, with gradually increasing fatigue and a fever that increases daily from low-grade to as high as by the third to fourth day of illness. Fever is commonly lowest in the morning, reaching a peak in late afternoon or evening. Headache, malaise, and anorexia Hepatosplenomegaly A transient, macular rash of rose-colored spots can occasionally be seen on the trunk.

TYPHOID FEVER
CLINICAL COURSE 10% of untreated patient excrete the bacteria in the feces for up to 3 months and some develop chronic carriage. - More common in women, infants and with biliary abnormalities.

TYPHOID FEVER
CLINICAL COURSE Development of severe disease depends on:
Host factors Strain virulence and inoculum Choice of antibiotic therapy

TYPHOID FEVER
DIAGNOSIS No specific diagnostic test other than culture DEFINITIVE DIAGNOSIS: ISOLATION or CULTURE
BEST: culture from blood or bone marrow (gold standard) 1st and 2nd wk blood (positive in more than 90% of affected individuals during the febrile phase) After 2nd week stool or urine Duodenal Aspirate not widely accepted due to poor tolerance

TYPHOID FEVER
DIAGNOSIS Serologic Tests
None are sufficiently sensitive or specific to replace culture based methods Felix-Widal Test, Typhidot Test

PCR and DNA probe assays

Identified but not yet developed for clinical use

TYPHOID FEVER
Serologic Tests Felix-Widal Test
Measures agglutinating antibody levels against O and H antigens May cross-react with other Enterobacteriacae Useful in areas that cannot afford the more expensive diagnostic tests Labor intensive and time consuming

TYPHOID FEVER
Serologic Tests Typhidot
Detects specific IgM and IgG antibodies to S.typhi Cannot differentiate acute/convalescent/reinfection IgG false (+)

TYPHOID FEVER
TREATMENT Prompt antibiotic administration
Choice depends on susceptibility of strain in a specific area Empirical treatment: CEFTRIAXONE Fully susceptible: CIPROFLOXAXIN AMOXICILLIN
Traditional 1st-line: Chloramphenicol, TMP-SMZ, Amoxicillin

MDR: CIPROFLOXACIN NAR: CEFTRIAXONE

TYPHOID FEVER
TREATMENT Uncomplicated Enteric Fever
managed at home with oral antibiotics and antipyretics

Persistent vomiting, diarrhea, and/or abdominal distention

Hospitalize; supportive therapy; 3rd gen ceph + fluoro

TYPHOID FEVER
TREATMENT Severe enteric fever
High dose IV dexamethasone + antimicrobials Reduced mortality for patients with high-risk of meningitis

Chronic carriers
Oral amox / TMP-SMZ / ciproflox / norfloxacin Anatomic abnormality surgical correction

TYPHOID FEVER
PREVENTION
Avoid risky foods and drinks
Boil it, cook it, peel it, or forget it.

Vaccination
For travelers to areas where there is an increased risk of exposure to S.Typhi. Do not protect against S. Paratyphi infection. Not 100% effective, and typhoid fever could still occur. Two typhoid vaccines are available
Oral live, attenuated vaccine (Ty21a) Vi capsular polysaccharide IM vaccine (Vi CPS)

TYPHOID FEVER
VACCINATION
Ty21a: given on days 1,3,5,7 & booster every 5 years (not given <6 years) Vi CPS: 1 dose & booster every 2 years (not given <2 years) Whole cell vaccine: no longer available due to higher incidence of side effects (esp. fever) Vi-rEPA: induced higher levels of IgG; not yet commercially available

TYPHOID FEVER
VACCINATION
Immunization is an adjunct and not a substitute for avoiding high-risk foods and beverages A high inocula can still overcome the protective efficacy of a vaccine

NON TYPHOIDAL SALMONELLOSIS (NTS)

Epidemiology
Incidence is highest during rainy season in tropical climates

and warmer months in temperate climates Increased risk of morbidity and mortality among the following:
Elderly Infants Immunocompromised individuals

NTS can be acquired from multiple animal reservoirs Transmission is commonly associated with food products

Centralization of food processing and widespread food

distribution also contributed to incidence of NTS

Epidemiology
Increased in antibiotic resistance is attributed to use of

antimicrobial agents in food animals

Highest seen in ampicillin followed by TMP-SMX

Broad spectrum antibiotics are the agents of choice

Pathogenesis
Almost similar to typhoid except that in NTS it is

characterized by infiltration of PMN. It involves both the small and large bowel mucosa. Degranulation and release of toxins of neutrophils results to inflammatory diarrhea.

Clinical Manifestations
Gastroenteritis
Nausea, vomiting & diarrhea occurs 6-48 hours Abdominal cramping and fever Rarely, pseudoappendicitis or inflammatory bowel diseases

Bacteremia and endovascular infections

8% NTS cases
Common among infants, elderly and immunocompromised

patients May be suspected in presence of high grade fever or preexisting bacteremia especially with heart diseases

Localized Infections
Intrabadominal Infections
Manifest as hepatic or splenic abscesses or cholecystitis

CNS Infections
Most common among infants 1-4 months old Rare infections ventriculitis & brain abscess

Pulmonary Infections
Usually presents with lobar pneumonia Complications may include empyema, lung abscess and fistula

formation

Urinary and genital tract Infections

Presents either with cystitis or pyelonephritis Risk factors include malignancy, HIV infection, renal transplantation

Localized Infections
Bones, Joints, Soft Tissue
Salmonella osteomyelitis most often associated with sickle cell

disease, pre existing bone disease Septic arthritis usually involving the knee, hip, shoulder joints Reactive Arthritis (Reiters syndrome) associated with persons with HLA-B27 antigen

Diagnosis
Isolation of the organism from stool, blood or other sterile

body fluids Echocardiography and CT scan may be indicated to identify localized infections Culture of joint fluid, abscess drainage and CSF may be done

Treatment
Symptoms are usually self-limited thus antibiotics must not be

routinely used In addition, antibiotics used has been associated with Increase rate of relapse and adverse drug reactions Preemptive treatment among those at increased risk
48-72 hours and among immunocompromised up to 7-14 days

Low grade bacteremia treated for 7-14 days

HIV/AIDS patients treated with IV antibiotics for 1-2 weeks then

oral antibiotics for 4 weeks Cases of relapse treated with long term suppressive therapy with TMP-SMX Endocarditis or arteritis for 6 weeks with B-lactam antibiotics