CJP's Abhijeet Dipke's typhoid diagnosis: Does suppressing a fever make a bacterial infection worse?

Abhijeet Dipke, founder of the Cockroach Janta Party (CJP), has been diagnosed with typhoid amid ongoing protests demanding the resignation of Education Minister Dharmendra Pradhan over the NEET-UG paper leak. The diagnosis marks a critical turn, given that Dipke has been on an indefinite hunger strike since July 18 under gruelling Delhi monsoon conditions.  It underscores how extreme physical exhaustion, sleep deprivation, and high cortisol levels systematically break down the body's defences.

What is typhoid? 

Typhoid is a serious type of bacterial infection that is caused by the bacteria known as Salmonella typhi. It causes a high fever that can last for weeks, belly pain, diarrhoea, and vomiting. It can lead to serious complications without treatment.

Typhoid fever is a life-threatening illness. 

How monsoon conditions trigger typhoid

According to Dr Rajmadhangi D., internal medicine specialist at Apollo Spectra Hospital, MRC Chennai, typhoid spreads rapidly through food and water contaminated by the bacteria during the monsoon season. 

"When an individual ingests typhoid-contaminated food or water, bacteria invade the digestive tract. The condition is associated with a continuing high fever and extreme weakness. Due to serious inflammation of the digestive tract, the pain in the abdomen feels normal. It is very important that typhoid is diagnosed at the early stages for appropriate treatment intervention," said Dr Rajmadhangi. 

Dipke, in a social media post, revealed his diagnosis and said that he would continue the protest till the education minister resigns. "Getting IV drips every morning," he said.

Meanwhile, before his official diagnosis on Saturday, Dipke admitted to running a severe fever and masking the symptoms with heavy doses of daily painkillers to stay on the field.

Why painkillers and paracetamol are not the cure for bacterial infection 

Paracetamol and NSAIDs are appropriate for symptom relief in infectious fever. Still, they do not treat the infection itself, and the evidence does not support routine use with the goal of improving cure. The main concern is not a dramatic “immune shutdown,” but a possible modest blunting of some inflammatory and febrile responses that may matter in selected infections or critically ill patients. 

Paracetamol is generally preferred when the main aim is to reduce fever or pain with less gastrointestinal, renal, and bleeding risk than NSAIDs. Available evidence suggests it can reduce fever and inflammation-related symptoms, but there is no convincing proof that usual short-course dosing meaningfully impairs infection clearance in typical outpatient viral or bacterial febrile illnesses. In critically ill patients, some studies have not shown outcome benefit from fever suppression, and a few observational signals have raised concern, but these data are not enough to establish harm from paracetamol itself. 

NSAIDs can be very effective for fever and inflammatory pain, but they carry more practical safety issues than paracetamol, including renal injury, gastric bleeding, and fluid retention, especially in dehydration, sepsis, or kidney disease. On immune effects, the literature suggests NSAIDs may alter cytokine signalling and inflammatory pathways, but whether this delays cure is not consistently demonstrated in real-world infection treatment. In some respiratory infections, symptom control with either paracetamol or NSAIDs is considered reasonable based on patient symptoms rather than any disease-modifying effect. 

For most infectious fevers, paracetamol and NSAIDs are supportive treatments, not infection treatments, and current evidence does not show that ordinary short-course use clearly prevents recovery. The stronger concern is safety selection—especially kidney, GI, and liver risk—rather than major immune suppression.