Langsung ke konten utama

Pathophysiology of Typhoid Fever

Pathophysiology of Typhoid Fever


Typhoid fever, also known as Typhoid, is a common worldwide illness, transmitted by the ingestion of food or water contaminated with the feces of an infected person, which contain the bacterium Salmonella enterica enterica, serovar Typhi. The bacteria then perforate through the intestinal wall and are phagocytosed by macrophages. The organism is a Gram-negative short bacillus that is motile due to its peritrichous flagella. The bacterium grows best at 37°C / 98.6°F – human body temperature.

This fever received various names, such as gastric fever, abdominal typhus, infantile remittant fever, slow fever, nervous fever, pythogenic fever, etc. The name of "typhoid" was given by Louis in 1829, as a derivative from typhus.

Pathophysiology of Typhoid Fever

Transmission of Salmonella typhi can be transmitted through various ways, which is known with 5 M of the Food Fingers, Fomitus (vomiting), Fly, and through Faeces.
Faeces and vomiting in patients with typhoid salmonella typhi can transmit the germ to others. Germs can be transmitted through the intermediary of flies, which fly will perch on the food to be eaten by healthy people. If the person is less attention to hygiene such as washing her hands and food contaminated with salmonella bacteria enter the body thypi a healthy person through the mouth. Then the germs get into the stomach, some bacteria will be destroyed by stomach acid and partly into the distal small intestine and reach the lymphoid tissue. In this lymphoid tissue breed germs, and then enter the bloodstream and reach the reticuloendothelial cells. Reticuloendothelial cells are then release germs into the bloodstream and cause bacteremia, bacteria then enter the spleen, small intestine and gallbladder.

Komentar

Postingan populer dari blog ini

Pathophysiology of COPD

COPD, or chronic obstructive pulmonary disease, is a progressive inflammatory disease connecting the airways, lung parenchyma, and vasculature. It causes the damage and remodeling of the airways and lung tissue. Proper functioning of lungs is rejected continuously by COPD. Over a period of time, these changes result in more severe conditions such as pulmonary hypertension and right heart failure. The precise pathophysiology of COPD is unidentified. The inflammatory process is a driving aspect in the pathophysiology of COPD. Recent verification suggests that the inflammatory response results in a number of effects, including an arrival of inflammatory cells such as macrophages, neutrophils and lymphocytes. Thickened airways and structural changes such as increased smooth muscle and fibrosis may also be manifested. Cigarette smoking causes an inflammatory response in the lungs. This response does not cease with the removal of the stimulus, but progresses for an unlimited period of time

Pathophysiology of Meningitis

Pathophysiology of Meningitis Predisposing factors include upper airway infection, otitis media, mastoiditis, sickle cell anemia and other hemoglobinopatis, a new neurosurgical procedure, head trauma and immunological effects. Venous channels through the posterior nasopharynx, middle ear and mastoid tract to the brain and the veins near the channel meningen; all of these links that support the growth of bacteria. Organisms enter the bloodstream and cause an inflammatory reaction in the meningen and under the cortex, which can cause thrombus and decreased cerebral blood flow. Cerebral tissue due to impaired metabolism meningen exudate, vasculitis and hypoperfusion. Purulent exudate may spread to the base of the brain and spinal cord. Inflammation also spread to the wall membrane of the cerebral ventricles. Bacterial meningitis associated with intracranial physiological changes, which consisted of increased permeability of the blood, the defense area of the brain, cerebral edema an