Typhoid Fever: diagnosis and complications

Typhoid Fever: diagnosis and complications

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Typoid fever is an acute enteric disease caused by an obligate intracellular bacillus called Salmonella Typhi and this bacillus resides within mononuclear phagocytic cells of lymphoid tissues. The disease is unique humans and it is characterized by fever, splenomegaly and neutropenia.

Transmission: Feco-oral routes through contaminated foods

Carriers

convalescent carrier – for up to 6 months of infection ·       

Chronic fecal and chronic urinary carriers are associated with chronic cholecystitis andpyelonephritis respectively.     

S. mansoni and S. hematobium co-infections protract the course of typhoid fever,

Pathogenesis:

Infection is by ingestion of the organism, (gt;10 to the power of 7 ) in 50% of cases penetrate the small intestine mucosa and reach the circulation with transient bactremia ·       

The bacilli are taken by the lymphatic to lymph nodes and they are engulfed by mononuclear phagocytic cells.

After a period of multiplication in these phagocytic cells, the organisms rupture the cells and invade the blood stream via the thoracic duct. The liver, gallbladder, spleen, kidney and bone marrow become infected during this second bactermic phase, characterizing the clinical features of the diseases.       

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The main pathological changes are found in the gastrointestinal tract particularly The Payer’s patches, which are the sub mucosal lymphoid follicles in this tract. This invasionarises from the gall bladder.

Payer’s patches may show:

Hyperplasia in first week

Necrosis in second week

Ulceration in third week

Healing in fourth week

Typhoid ulcers are oval and are situated longitudinally along the long axis of the colon, which are in contra -distinction of tuberculous ulcers that are set transversally.

Diagnosis

Leukopenia 3000-4000/mm3

Blood culture – 1st week (70-90%) Fecal culture – 2nd – 3rd week best (75%)

Urine culture – 2nd – 3rd week

Serology 2nd week Typhoid fever is a protracted disease that is associated with bactermia, fever and chills during the first week

Widespread reticuloendothelial involvement with rash, abdominal pain and prostration in the second week and

Ulceration of payer’s patches with intestinal bleeding and shock during the third week

Complications may include

Intestinal perforation: 3 – 4% and it is responsible to 25% of the death ·        Intestinal hemorrhage: 8% and usually seen between 14-21 days of illness Acute cholecystitis

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