Typhoid/Enteric fever

Enteric fever is a systemic syndrome produced by a group of certain Salmonella organisms Typhoid feverS.Typhi paratyphoid feverS.paratyphi- A,B or C

 Background: Typhoid fever, also known as enteric fever, is a systemic infection/syndrome by Salmonella typhi or Salmonella paratyphi A,B,C(less virulent). Since ancient times, these bacteria have thrived during wartime and during the breakdown of basic sanitation. S typhi :developing nations where sanitation is generally poor. Sporadic outbreaks occur in developed nations, H/O travel to endemic areas

Epidemiology
Of all Salmonella serotypes, only S typhi and S paratyphi are pathogenic exclusively in humans. Typhoid fever is potentially fatal if untreated Humans are the only natural reservoir , so direct or indirect contact with an infected person (sick/carrier) is necessary for inf

Mode of transmission
1)Ingestion of food or water contaminated with human excreta/sewage-most common 2)Water borne outbreaks - poor sanitation 3) direct fecal-oral spread - poor personal hygiene 4)Oysters and shellfish cultivated in water (1) 5) International travellers to Asia, Latin America 6)Cong transmission-transplacental or intrapartum

Pathogenesis
After ingestion the bacilli reach the intestine, passing the gastric barrier. Attach to the microvilli of the ileal brush border & invade the intestinal epth thru the peyers patches Reach the int lymph nodes,multiply within the mononuclear cells Monocytes unable to destroy the org.in early stages of the dis.carry them to the mesenteric lymph nodes and

 Thru the thoracic duct reach the blood stream transient bacteremia Reach the RES and other organs& proliferate bacteremia recurs

Pathogenesis
Hyperplasia of the peyers patches with necrosis &sloughing of the epithelium, produce ulcers(longitudinal) that may bleed, but heal without scarring. The inflammatory lesion may penetrate the muscularis and the serosa of the intestines perforation

 Mesenteric lymph nodes, liver, gall bladder(GB) and spleen are inflammed with focal necrosis. Local multiplication of the organism in the walls of GB large no. of salmonellaintestines Hyperplasia of the reticuloendothelial tissues with proliferation of mononuclear cells is the predominant finding, areas of focal necrosis

 After a period of transient bactremia, the bacilli r seeded in various organs, liver, spleen, gallbladder, & bonemarrow, further multiply This phase heralds the onset of clinical illness. Bile serves a good culture media for the org to continue multiplying and the gall bladder discharges large no. of org. into the intestines Peyers patches and other lymphoid follicles get inflammed and slough off to form typhoid ulcers and lead to the 2 most dreaded complications , hemorrhage and perforation

 Salmonellae are grouped based on the somatic O antigen and further divided into serotypes based on flagellar H and surface virulence (Vi) antigens. S typhi, the cause of typhoid fever, has O and H antigens, an envelope (K) antigen, and a lipopolysaccharide macromolecular complex called endotoxin that forms the outer portion of the cell wall. S typhi, S paratyphi C, and Salmonella Dublin are the only Salmonella serotypes that carry Vi antigen

 It is an imp public health problem Recently it has developed increasing bact resistance to various antibiotics Gram negative bacilli,motile and have flagella. They possess flagellar antigen H and somatic antigen O

 Epidemiology: S.typhi occurs only in humans Transmission: feco oral route ,thru contaminated water or food Acutely infected patients excrete bacilli in their stool or urine for a variable period 5% of the adults become chronic carriers (resevoir)

 Food handlers and cooks are potent source of infection Most of the infected children stop excreting the bacilli within 2 -3 mths and rarely become carriers Epidemics occur : contaminated drinking water, poor sanitation and personal hygiene, overcrowding & poverty

 Older children & young adults most infected ,10% occur in under 5s and 1-2% below 2yrs of age

Clinical picture
Incubation period: 7- 14 days, (3-30days) Clinical manifestations depend on age: school-age &adolescents: First week: Onset is insidious, fever, malaise, anorexia, myalgia, headache &abd pain over a period of 2 3 days,(more severe in the 2nd week) Diarrhea-pea soup consistency initially, later constipation is prominent

 Temp rises in a step ladder pattern, becomes unremitting ,high within a week

Second week: By the end of the first week- a soft small splenomegaly,often with S/S of bronchitis Mild jaundice , right hypochodrial pain (acalculous cholecystitis),hepatomegaly Sign of meningism (no meningitis) Fever sustained with relative bradycardia Distended abdomen,diffuse tenderness

 Rose spots in 50% cases ,macular or maculopapular,discreet,erythematous,1-5 mm, blanch on pressure Appear in crops ,10-15 on the lower chest and abdomen, last for 2 -3 days,culture of the lesion positive for S.Typhi Rhonchi and rales on auscultation If no complications ,resolve in 2- 4 weeks

 Malaise and lethargy may persist for 1-2 mths Patient may be emaciated by the end of the illness enteric fever by non typhoidal salmonella is milder

 Infants and young children: RARE, milder, present as acute gastroenteritis, LRTI, or VF Neonates: transmission is vertical. Begins within 3 days of delivery.vomiting, diarrhea, and abd distension are common. temp variable 40.5 C seizures, hepatomegaly, jaundice, wt. loss

 Diagnosis: Culture of the organism is the basis 1st week: Blood culture 2nd week: Agglutination test 3rd week: Stool culture 4th week: Urine culture BASU

 LAB FINDINGS:anemia, normochromic, normocytic blood loss/bonemarrow depression Leucopenia , never below 2,500 leucocytosis,20,000-25,000(abscess) Thrombocytopenia LFT deranged Proteinuria PUS &RBCs in stool

D/D: GE VF BRONCHITIS /BP LATER ; SEPTICEMIAS ANICTERIC HEPATITIS LEUKEMIAS /LYMPHOMAS

Treatment
Antibiotic is essential for treating enteric fever. The fluoroquinolones and third generation cephalosporins are the current mainstay of therapy. Ceftriaxone recommended for ped age grp 80mg/kg/day in a single dose Relapse rate is low and prevents carrier state

 Quinolones have the adv of dose and cost effective Probable toxic effect on growing cartilage, not recommended A short course of steroids improves the survival rate of patients with shock, obtundation, stupor/coma. initial dose of dexamethasone 3mg/kg followed by 1mg/kg 6 hrly for 48 hrs

 Supportive treatment & maintenace of fluid and electrolytes , Surgical intervention Blood transfusion Diet

Complications
Intestinal hemorrhage & perforation after the first week Hemorrhage : drop in temp &blood pressure increase in pulse rate Perforation : marked increase in abd pain, tenderness, vomiting& signs of peritonitis. Pneumonias : superinf Toxic myocarditis, myogenic shock

 Neurological :increased intracranial tension, thrombosis, ataxia, chorea, aphasia, deafness, psychosis& transverse myelitis. Permanent sequlae are rare. Osteomyelitis and septic arthritis are more common in kids with hemoglobinopathies

Prognosis
Depends on prompt therapy, age, previous state of health, Salmonella serotype and the appearance of complications In developing coutries , mortality rate is higher 10%. Relapse known to occur in untreated cases, (numerous), milder, shorter duration

Carriers : Risk is low in kids and increases with age Patients who excrete S.typhi @ 3mths or longer,are excretors @ one yr &defined as chronic carriers. Incidence of biliary tract dis is higher.

Prevention
Improved sanitation & clean water, essential Personal hygiene measures, handwashing, Attention to food prep practice Course of 4-6 wks of high dose ampicillin (amoxycillin) plus probenecid or TMX-SMX Ciproflox in adults, cholecystectomy

 Vaccines:3 types available Parenteral , inactivated vaccine confers limited protection(50-75%) ass with side effects. Approved for children 6 mths and above 2 doses (0.25ml -6mths-10yrs) &( 0.5mlabove 10yrs),S/C, 4 weeks apart. Boosters every 3 yrs necessary

 Oral live vaccine Ty21a strain (80%) Three capsules given on alternate days, repeated every 3yrs Not recommended <6ys

 Vi polysacch typhoid vaccine : Vi antigen is a capsular antigen Effective after the age of 2 yrs 0.5 ml I/M deltoid area ,booster 2-3 yrs yrs