Infectious Diseases

Learning Objectives

By the end of this topic, you should be able to:

• Define sepsis and septic shock using the current (Sepsis-3) criteria
• Recognize the early clinical features of sepsis and apply the "Sepsis Six" bundle within the first hour
• Differentiate the common bacterial and viral infections seen in general medicine by presentation and first-line treatment
• Explain the principles of antimicrobial stewardship and why inappropriate antibiotic use drives resistance
• List the routine diagnostic tests used to identify an infectious agent and interpret them in context
• Identify red-flag features that separate a self-limiting infection from a life-threatening one

Quick Answer

Infectious diseases are illnesses caused by pathogens — bacteria, viruses, fungi, or parasites — invading and multiplying in the body. Most are self-limiting, but some, like untreated bacterial infections, can progress to sepsis, a life-threatening state where the body's response to infection injures its own organs. Recognizing sepsis early (using red flags like altered mental status, low blood pressure, and high respiratory rate) and starting the "Sepsis Six" within an hour dramatically improves survival. Equally important is antimicrobial stewardship — using antibiotics only when needed, at the right dose and duration — because overuse breeds resistant organisms that make future infections harder to treat. This topic matters because infections are the single most common reason patients present acutely to hospital, and getting the first hour right saves lives.

Sepsis: The Core Emergency

What is sepsis?

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. This is the modern (Sepsis-3, 2016) definition — the key insight is that it isn't the infection itself that kills the patient, it's the body's own inflammatory and coagulation cascades running out of control, causing capillary leak, hypotension, and organ hypoperfusion.

Septic shock is a subset of sepsis where circulatory and cellular/metabolic abnormalities are severe enough to substantially increase mortality — clinically, this means persistent hypotension requiring vasopressors to maintain a mean arterial pressure ≥65 mmHg, plus a serum lactate >2 mmol/L despite adequate fluid resuscitation.

How to recognize it

Bedside screening tools help flag patients early:

• qSOFA (quick Sequential Organ Failure Assessment) — any 2 of: respiratory rate ≥22/min, altered mentation (GCS <15), systolic BP ≤100 mmHg. A positive qSOFA outside ICU should prompt escalation and lactate measurement, though it's a prompt, not a diagnostic test.
• NEWS2 (National Early Warning Score) is used more widely in UK/Indian hospitals as it's more sensitive for deterioration.
• Full SOFA score (looking at respiratory, cardiovascular, hepatic, coagulation, renal, and neurological systems) confirms organ dysfunction in the context of suspected/confirmed infection.

Why it exists as a distinct entity

Before Sepsis-3, "SIRS" (systemic inflammatory response syndrome — fever, tachycardia, tachypnea, abnormal white count) was used to define sepsis. SIRS was too sensitive and non-specific (a person with the flu meets SIRS criteria) and didn't correlate well with mortality. Sepsis-3 shifted the focus to organ dysfunction, which is what actually predicts death.

Management: the Sepsis Six

Within the first hour of recognizing sepsis, give three and take three:

Give:

1. High-flow oxygen (target SpO2 94-98%)
2. IV fluids (30 mL/kg crystalloid bolus if hypotensive or lactate ≥4 mmol/L)
3. IV broad-spectrum antibiotics (empirical, per local protocol, within the first hour — every hour of delay increases mortality)

Take:

1. Blood cultures (ideally before antibiotics, but never delay antibiotics to get them)
2. Serum lactate
3. Urine output monitoring (catheterize if needed)

If the patient remains hypotensive after fluid resuscitation, they need vasopressors (noradrenaline is first-line) and ICU-level care — this defines septic shock.

Real-world example: A 68-year-old diabetic presents with fever, confusion, and a systolic BP of 88 mmHg after three days of dysuria. His qSOFA is 2/3 (altered mentation, low BP). Urine dipstick suggests a UTI. This is presumed urosepsis until proven otherwise — he needs the Sepsis Six started immediately, not a wait for urine culture results.

Common misunderstanding: Students often think sepsis requires a positive blood culture. It doesn't — sepsis is a clinical syndrome. Many patients with clear septic shock have negative cultures (culture-negative sepsis is common, especially if antibiotics were given before samples were taken).

Common Bacterial Infections

Definition and overview

Bacterial infections are caused by single-celled prokaryotic organisms multiplying in host tissue. Unlike viruses, most bacteria can be grown on culture media and targeted with antibiotics that exploit differences between bacterial and human cell biology (cell wall synthesis, protein synthesis machinery, DNA replication enzymes).

Infection	Typical organism	Classic presentation	First-line treatment
Community-acquired pneumonia	Streptococcus pneumoniae	Fever, productive cough, pleuritic chest pain, consolidation on CXR	Amoxicillin (mild) or amoxicillin + macrolide (moderate-severe), per CURB-65
Urinary tract infection	E. coli (most common)	Dysuria, frequency, suprapubic pain; fever/flank pain if pyelonephritis	Nitrofurantoin or trimethoprim (uncomplicated); IV ceftriaxone if pyelonephritis
Cellulitis	Streptococcus pyogenes, Staphylococcus aureus	Spreading erythema, warmth, tenderness, poorly demarcated edge	Flucloxacillin (or clindamycin if penicillin-allergic)
Tuberculosis	Mycobacterium tuberculosis	Chronic cough >2-3 weeks, night sweats, weight loss, hemoptysis	RIPE regimen (Rifampicin, Isoniazid, Pyrazinamide, Ethambutol) for 2 months, then RI for 4 months
Bacterial meningitis	Neisseria meningitidis, S. pneumoniae	Fever, neck stiffness, photophobia, non-blanching rash (meningococcal)	Empirical IV ceftriaxone immediately, before LP if patient unstable

Why it matters: Recognizing the pattern (organism + typical site + typical patient) lets you start rational empirical therapy before culture results return two to three days later — a delay that would be dangerous in meningitis or sepsis.

Common misunderstanding: Not every fever with a raised white cell count is bacterial. Viral infections can also raise inflammatory markers modestly. The strongest bacterial pointers are a very high or very low white cell count, high CRP/procalcitonin, and a clearly localizing source (e.g., consolidation, pyuria).

Common Viral Infections

Viruses are obligate intracellular parasites — they cannot replicate without hijacking a host cell's machinery, which is why antivirals are harder to design (they must target viral, not human, processes) and why most viral illnesses are managed supportively.

Infection	Organism	Key features	Management
Influenza	Influenza A/B	Abrupt fever, myalgia, headache, dry cough	Supportive; oseltamivir if high-risk and within 48 hours of onset
Dengue	Dengue virus (flavivirus)	High fever, retro-orbital pain, rash, thrombocytopenia; warning signs = abdominal pain, bleeding, plasma leakage	Supportive care, careful fluid management, platelet monitoring
Viral hepatitis (A/B/C)	Hepatitis viruses	Jaundice, malaise, deranged LFTs; Hep B/C can become chronic	Supportive for Hep A; antivirals (tenofovir, direct-acting antivirals) for chronic Hep B/C
HIV	Human immunodeficiency virus	Acute seroconversion illness (flu-like), then latency, then AIDS-defining illnesses if untreated	Lifelong antiretroviral therapy (ART) — now started immediately after diagnosis regardless of CD4 count
COVID-19	SARS-CoV-2	Fever, cough, anosmia, dyspnea in severe disease	Supportive; dexamethasone and/or antivirals in hypoxic patients

Why it matters: Distinguishing a viral from a bacterial illness prevents unnecessary antibiotic prescriptions — a central pillar of antimicrobial stewardship.

Antimicrobial Stewardship

Definition

Antimicrobial stewardship is the coordinated set of practices designed to ensure antibiotics (and other antimicrobials) are prescribed and used only when needed, at the correct dose, via the correct route, for the correct duration.

Why it exists

Every course of antibiotics exerts selection pressure — bacteria that survive (through resistance genes, efflux pumps, or altered targets) go on to multiply and spread. Overuse and misuse (treating viral infections, prolonged "just in case" courses, wrong drug for the organism) accelerates the emergence of multidrug-resistant organisms like MRSA, ESBL-producing E. coli, and carbapenem-resistant Enterobacteriaceae (CRE) — infections that may become untreatable with current drugs.

How it works in practice

• Culture before (or alongside) starting antibiotics, then de-escalate from broad-spectrum to narrow-spectrum once sensitivities return
• Review at 48-72 hours ("antibiotic time-out") — stop if not needed, switch IV to oral when the patient is stable (IV-to-oral switch)
• Fixed, evidence-based durations rather than open-ended courses (e.g., 5-7 days for most uncomplicated UTIs, not 14)
• Avoid antibiotics for self-limiting viral illnesses (most upper respiratory tract infections, uncomplicated viral gastroenteritis)
• Source control — draining an abscess or removing an infected line matters as much as the drug choice; antibiotics alone won't work if the source isn't controlled

Real-world example: A patient with mild community-acquired pneumonia is started on amoxicillin. At 48 hours she is afebrile and cultures show a penicillin-sensitive pneumococcus. Stewardship means keeping her on the narrow-spectrum amoxicillin rather than "upgrading" to a broad-spectrum agent, and stopping at 5 days rather than extending the course by default.

Common misunderstanding: Many students (and patients) believe you must always "finish the course" no matter the length originally prescribed. Current evidence-based guidance is that shorter, well-chosen courses are often just as effective as longer ones and reduce resistance pressure — the real rule is "take antibiotics exactly as prescribed," and prescribers should be prescribing evidence-based shorter durations in the first place.

Diagnosis of Infectious Diseases

Diagnosis combines clinical assessment with targeted investigations:

• Cultures (blood, urine, sputum, wound) — the gold standard for identifying the organism and its sensitivities, but takes 24-72 hours
• Molecular tests (PCR) — rapid detection of viral or bacterial DNA/RNA, useful when speed matters (e.g., meningitis panels, COVID-19)
• Serology — detects antibodies to a pathogen, useful for past exposure or infections where the organism is hard to culture (e.g., hepatitis, HIV, dengue)
• Inflammatory markers — CRP, procalcitonin, white cell count — support the diagnosis and can track response to treatment, but are not organism-specific
• Imaging — chest X-ray for pneumonia, CT/MRI for deep-seated collections

Key Terms

Term	Definition
Sepsis	Life-threatening organ dysfunction caused by a dysregulated host response to infection
Septic shock	Sepsis with persistent hypotension needing vasopressors plus lactate >2 mmol/L despite fluid resuscitation
qSOFA	Bedside screening score (respiratory rate, mental status, systolic BP) used to flag possible sepsis outside ICU
SIRS	Older criteria (fever, tachycardia, tachypnea, abnormal WBC) once used to define sepsis; now considered too non-specific
Empirical therapy	Antibiotic treatment started based on the most likely organism, before culture results are available
De-escalation	Narrowing antibiotic spectrum once culture and sensitivity results identify the specific organism
Antimicrobial stewardship	Coordinated practices ensuring antimicrobials are used only when needed, correctly dosed, and for the right duration
Antimicrobial resistance	The ability of a microorganism to survive exposure to a drug that would normally kill or inhibit it
Culture-negative sepsis	Clinically diagnosed sepsis where blood cultures fail to grow an organism, often because antibiotics were given first
Source control	Physical measures (drainage, debridement, device removal) to eliminate the focus of infection alongside antibiotics

Common Mistakes

Misconception 1: "Sepsis is just a severe infection with a high fever." Why it's wrong: Sepsis is defined by organ dysfunction, not by temperature or the severity of the infection itself. A patient can be septic while hypothermic and afebrile, especially the elderly or immunosuppressed. Correct understanding: Look for signs of organ dysfunction — confusion, low urine output, hypotension, raised lactate — not just how "sick" the infection looks.

Misconception 2: "You must wait for blood culture results before starting antibiotics in suspected sepsis." Why it's wrong: This delay increases mortality — each hour of delayed antibiotics in septic shock is associated with a measurable rise in death rate. Correct understanding: Take cultures if possible, but never delay empirical antibiotics beyond the first hour to wait for them.

Misconception 3: "Every patient should complete a long, standard course of antibiotics to be safe." Why it's wrong: Unnecessarily long courses don't improve cure rates for most common infections and directly contribute to antimicrobial resistance. Correct understanding: Use the shortest evidence-based duration for the specific infection, and review/stop early if clinical improvement and cultures allow.

Comparison and Connections

Feature	SIRS (old criteria)	Sepsis (Sepsis-3)	Septic shock
Core requirement	≥2 of: fever/hypothermia, tachycardia, tachypnea, abnormal WBC	Suspected/confirmed infection + organ dysfunction (SOFA rise ≥2)	Sepsis + vasopressor-dependent hypotension + lactate >2 mmol/L
Specificity for mortality	Low — many non-infectious conditions trigger SIRS	Higher — correlates with actual organ injury	Highest — identifies the sickest subgroup
Clinical use today	Largely replaced	Current standard definition	Current standard definition
Immediate action	Investigate cause	Start Sepsis Six within 1 hour	Sepsis Six + vasopressors + ICU

Feature	Bacterial infection	Viral infection
Causative organism	Free-living single-celled prokaryote	Obligate intracellular particle
Typical treatment	Antibiotics (target cell wall, ribosomes, DNA gyrase)	Mostly supportive; specific antivirals for some (influenza, HIV, hepatitis)
Diagnostic gold standard	Culture and sensitivity	PCR or serology
Stewardship relevance	Risk of resistance if antibiotics misused	Antibiotics should NOT be given unless secondary bacterial infection suspected

Practice Questions

Recall

1. What are the two components that define septic shock according to Sepsis-3? Answer guidance: Persistent hypotension requiring vasopressors to maintain MAP ≥65 mmHg, AND a serum lactate >2 mmol/L despite adequate fluid resuscitation.

2. Name the three "give" and three "take" actions in the Sepsis Six. Answer guidance: Give — oxygen, IV fluids, IV antibiotics. Take — blood cultures, lactate, urine output monitoring.

Understanding

3. Explain why the Sepsis-3 definition replaced the older SIRS criteria. Answer guidance: SIRS was overly sensitive and non-specific (met by many non-infectious and self-limiting conditions) and didn't correlate well with mortality. Sepsis-3 focuses on organ dysfunction, which is the actual driver of death, giving better prognostic accuracy.

4. Why can a patient have clinically obvious septic shock but negative blood cultures? Answer guidance: Sepsis is a clinical syndrome, not a laboratory diagnosis. Cultures can be negative due to prior antibiotic exposure, low bacterial load, fastidious organisms, or non-bacterial causes of the same organ-dysfunction picture.

Application

5. A 74-year-old man is brought in confused, RR 26/min, BP 92/58, with a possible chest source. Walk through your first-hour management. Answer guidance: Recognize qSOFA positive (RR, BP, confusion) → treat as sepsis until proven otherwise → start Sepsis Six within the hour: oxygen, IV fluids (30 mL/kg if hypotensive), empirical broad-spectrum IV antibiotics for likely pneumonia; take blood cultures, lactate, monitor urine output; reassess response to fluids and escalate to vasopressors/ICU if lactate remains high or BP doesn't respond.

6. A patient with a mild sore throat and clear coryza asks for antibiotics "to be safe." How would you respond using stewardship principles? Answer guidance: Explain the illness is most likely viral (self-limiting URTI), that antibiotics won't help and carry side-effect and resistance risks, and give safety-netting advice for red flags (worsening fever, difficulty swallowing/breathing) that would warrant reassessment.

Analysis

7. Compare the reasoning behind empirical antibiotic choice versus de-escalation after culture results — why are both necessary, not contradictory? Answer guidance: Empirical therapy is needed because waiting for culture results (24-72 hours) in a potentially life-threatening infection is unsafe; it's based on the most likely organism and local resistance patterns. De-escalation is then necessary once the actual organism and sensitivities are known, to narrow the spectrum, reduce side effects, and limit resistance pressure — the two steps work together across the timeline of one illness.

8. A hospital sees rising rates of ESBL-producing E. coli. Analyze how prescribing practices might be contributing, and propose two stewardship interventions. Answer guidance: Contributing factors could include prolonged broad-spectrum antibiotic courses, lack of de-escalation once sensitivities are known, and treating asymptomatic bacteriuria unnecessarily. Interventions: implement a 48-72 hour antibiotic review/time-out policy, and restrict broad-spectrum agents (e.g., carbapenems, third-generation cephalosporins) to require specialist approval or culture-confirmed indication.

FAQ

Q1: Is sepsis the same thing as an infection spreading to the blood (bacteremia)? No. Bacteremia means bacteria are present in the blood; sepsis is the body's dysregulated response causing organ dysfunction. You can have bacteremia without sepsis, and sepsis without a positive blood culture.

Q2: Why is lactate measured in suspected sepsis? Lactate rises when tissues are under-perfused and shift to anaerobic metabolism. It's a marker of how sick the patient's circulation actually is, and a lactate that fails to fall despite fluids signals ongoing tissue hypoperfusion — hence its role in defining septic shock.

Q3: If cultures come back negative, should antibiotics be stopped? Not automatically. Clinical judgment matters — if the patient's picture strongly suggests infection and they're responding to treatment, antibiotics are often continued; negative cultures are common in genuinely septic patients, especially after pre-treatment.

Q4: Why don't antibiotics work on viral infections at all? Antibiotics target bacterial-specific structures (cell walls, bacterial ribosomes, bacterial enzymes) that viruses simply don't have — viruses hijack the host's own cellular machinery, so there's no bacterial target to hit.

Q5: How does antimicrobial resistance actually develop within a patient's course of treatment? Antibiotics kill susceptible bacteria, but any bacteria with pre-existing resistance mutations or genes survive and multiply unopposed, especially if the drug or duration was inadequate. Over time and across many patients, resistant strains become dominant and can spread person-to-person.

Quick Revision

• Sepsis-3 definition: life-threatening organ dysfunction from a dysregulated host response to infection — not just "a bad infection"
• Septic shock = sepsis + vasopressor-requiring hypotension + lactate >2 mmol/L despite fluids
• qSOFA (RR ≥22, altered mentation, SBP ≤100) is a bedside screening tool, not a diagnostic test
• SIRS criteria are outdated for defining sepsis due to poor specificity
• Sepsis Six (give: O2, fluids, antibiotics; take: cultures, lactate, urine output) must start within 1 hour
• Never delay empirical antibiotics to wait for culture results in suspected sepsis
• Bacterial infections respond to antibiotics targeting cell wall/ribosome/DNA machinery; viruses need supportive care or specific antivirals
• Common bacterial patterns: pneumococcus (pneumonia), E. coli (UTI), S. pyogenes/S. aureus (cellulitis), M. tuberculosis (TB), meningococcus (meningitis)
• Antimicrobial stewardship = right drug, right dose, right duration, right route — review at 48-72 hours and de-escalate
• Culture-negative sepsis is common and does not rule out the diagnosis
• Source control (draining abscesses, removing infected lines) is as important as antibiotic choice
• Shorter, evidence-based antibiotic courses are generally as effective as longer ones and reduce resistance

Related Topics

Prerequisites

• Basic microbiology (bacteria vs. viruses vs. fungi vs. parasites)
• Normal vital sign ranges and basic physiological monitoring
• Principles of the inflammatory response

Related Topics

• Fungal and parasitic infections
• Modes of disease transmission and infection control
• Vaccination and immunization schedules
• Fever of unknown origin

Next Topics

• Specific organ-system infections (pneumonia, meningitis, endocarditis) in depth
• Immunocompromised host infections (HIV-related opportunistic infections)
• Hospital-acquired and multidrug-resistant infections