TYPHOID (ENTERIC) FEVER
Dr. Aishwarya kumar
DR. AISHWARYA KUMAR
MEDICAL OFFICER
ASSISTANT COMMANDANT
CENTRAL RESERVE POLICE FORCE
DR. AISHWARYA KUMAR
ASSISTANT COMMANDANT
MEDICAL OFFICER
CRPF
Dr. Aishwarya Kumar
Medical Officer
Assistant Commandant
69 Bn. CRPF
Dr. Aishwarya Kumar
Medical Officer
Assistant Commandant
69 Bn. Central Reserve Police Force
TYPHOID FEVER OR ENTERIC FEVER
● Typhoid fever, or enteric fever, is a potentially fatal multisystemic infection
produced primarily by Salmonella enterica serotype typhi and to a lesser extent
Salmonella enterica serotypes and paratyphi A, B,C
● Salmonella are motile enterobacteriaceae produce a variety of gastrointestinal
infections ,presents in a wide variety of ways ranging from an overwhelming
septic illness to minor cases of diarrhea with low-grade fever. The classic
presentation is one of fever, malaise, diffuse abdominal pain, and constipation.
● Untreated typhoid fever may progress to delirium, obtundation, intestinal
hemorrhage, bowel perforation, and death within 1 month of onset
● Greek word for cloud, to emphasize the severity and long lasting
neuropsychiatric effects among the untreated.
1. AGENT FACTORS
● S typhi has a Vi capsular antigen that masks PAMPs, avoiding neutrophil-
based inflammation
● Specialised fimbrae
● Able to resist pH as low as 1.5
● Quorum Sense
Antigenic structure
There are two sets of antigen - detected by serotyping :
● Somatic or O Antigen : LPS ( long chain polysaccharide ) - Heat stable
polysaccharide .
● Flagellar or H Antigen : are strongly immunogenic and induces antibody
formation rapidly and in high titres following infection or immunisation .
PATHOPHYSIOLOGY
● Ingestion > Stomach > Small Intestine(P.P) > Mesenteric L.N > Thoracic Duct >
Liver/ spleen / Bone > Apoptosis > Bacteraemia > Small Intestine re -infection . Stool
and urine
● S typhi and paratyphi enter the host from distal ileum. They have specialized fimbriae
that adhere to the epithelium over clusters of lymphoid tissue in the ileum (Peyer
patches), here macrophages are traveling from the gut into the lymphatic system.
● S typhi has a Vi capsular antigen that masks PAMPs, avoiding neutrophil-based
inflammation but not seen in paratyphi A . Hence greater infectivity of Typhi as
compared with paratyphi isolates . Quorum Sense.(swarming + biofilm) + pH 1.5
resistance.
● Use macrophages machinery and multiply
Pathophysiology
Typhoid Bacilli Reach to small intestine Penetrate mucosa
Enters intestinal lymphatic
Blood stream
Disseminated
Re-enters bloodstream bacteraemia
CLINICAL FEATURES
● 1st Week : Malaise , headache , stepladder fever, dull frontal headache ,coated tongue, dry
cough, bloating , diffuse abdominal pain and tenderness and, colicky right upper quadrant
pain. Inflamed Peyer patches narrow the bowel lumen causing constipation .
● 2nd Week : 7 - 10 day Rose spots , mild hepatosplenomegaly is common , Relative
bradycardia + dicrotic pulse
● 3rd Week : Weight loss , “Typhoid state” - apathy, confusion and even psychosis, crackles
over the lung bases. Some experience foul, green-yellow, liquid diarrhea (pea soup
diarrhea). Necrotic Peyer’s patches may lead to bowel perforation and peritonitis .
ROSE SPOTS
COMPLICATIONS OF TYPHOID
● General- Toxaemia , DIC , Shock
● GIT- Perforation of intestine , Intestinal haemorrhage( 3 rd or 4th week of illness)
● Neurological – Delirium, Psychosis, Coma, Meningitis, Encephalopathy , peripheral
neuritis , Deafness
● Miscellaneous-
Myocarditis,Cholecystitis,Endocarditis,Pericarditis,Glomerulonephritis, Osteomyelitis
,Pneumonia, Hepatitis
DIAGNOSIS
Culture and sensitivity -
● Bone Marrow culture > 80 % sensitive
● Intestinal secretions culture
● Blood culture , stool culture and urine culture
Blood culture- During 1st week
Stool culture – During 3rd week
Urine culture – During 4th week
● If blood , bone marrow,and intestinal secretions are cultured yield is >90%
● Tells about the bacterial serotype and drug sensitivity .
INVESTIGATIONS
● CBC – Leucopenia with relative lymphocytosis
● The classic Widal serologic test for “febrile agglutinins” is simple and rapid but has limited
sensitivity and specificity, especially in endemic regions. Rapid point-of-care tests that detect
antibodies to outer-membrane proteins or to Vi or O:9 antigen are available for detection of S.
Typhi; they are moderately sensitive and specific, but their cost and accuracy have limited their
routine use in developing countries.
● Widal test – Detects antibodies to O, H and Vi antigens of S. paratyphi A, and B, other Salmonella
species.Antibodies against the O antigen are predominating IgM, rise early in the illness and disappear
early.
● In the absence of recent immunisation, a high titre of O antibodies (= 1:320) is useful, but not specific
for typhoid.
● The H antigen are flagellar antigens of Salmonella typhi, paratyphi A and B. Antibodies to H antigens
are both IgM and IgG, rise late in the illness and persist for longer time.
Other Serological tests:
● Typhi dot- detects IgM and IgG antibodies ( against a outer membrane protein)
● Molecular methods – PCR to detect flagellin, somatic gene, Vi gene.
Treatment
● Mainstay are Antibiotics and initial choice depends on susceptibility .
● DOC for drug-susceptible typhoid fever is fluoroquinolones but due to high prevalence of
ciprofloxacin resistance in Indian subcontinent , not used for empirical treatment .
● Over the years, it has developed increasing resistance to antibiotics. During 2016,
extensively drug-resistant typhoid (XDR) were documented in Pakistan. Only three
classes of antimicrobial agents, azithromycin, carbapenems, and tigecycline, remain
affective among these strains.
PREVENTION
