Bacterial infections
Bacterial infections for FCPS: typhoid, cholera, meningitis, pneumonia, endocarditis
Typhoid, cholera, meningitis, pneumonia, endocarditis, rheumatic fever, tetanus, diphtheria and other key bacterial infections for FCPS Part 1. For each, learn the stain, how it causes disease, the classic picture, the lab clue and the drug of choice.
Sorting bacteria
| Group | Examples |
|---|---|
| Gram-positive cocci | Staphylococcus (clusters, catalase positive); Streptococcus and Enterococcus (chains or pairs, catalase negative) |
| Gram-positive rods | Clostridium (anaerobic, spores), Corynebacterium, Listeria, Bacillus |
| Gram-negative cocci | *Neisseria meningitidis*, *N. gonorrhoeae*, Moraxella |
| Gram-negative rods | Enterobacteria (*E. coli*, Salmonella, Shigella, Klebsiella, Proteus), Pseudomonas, Burkholderia, Vibrio, Haemophilus, Bordetella, Brucella, Legionella, Helicobacter, Fusobacterium (anaerobe) |
| No cell wall / intracellular / spiral | Mycoplasma; Chlamydia, Rickettsia; Treponema, Leptospira, Borrelia |
How bacteria cause disease: toxins
| Toxin | Organism | Action | Result |
|---|---|---|---|
| Cholera toxin | *Vibrio cholerae* | Locks Gs on, raising cAMP; CFTR pours out chloride and water | Painless rice-water diarrhoea |
| Heat-labile toxin | Enterotoxigenic *E. coli* | Same as cholera | Traveller's diarrhoea |
| Shiga toxin | Shigella, *E. coli* O157:H7 | Inactivates the 60S ribosome | Dysentery, haemolytic uraemic syndrome |
| Diphtheria toxin | *Corynebacterium diphtheriae* | ADP-ribosylates elongation factor 2, stopping protein synthesis | Pseudomembrane, myocarditis, palatal and other nerve palsies |
| Tetanospasmin | *Clostridium tetani* | Blocks glycine and GABA release from inhibitory interneurons | Spastic paralysis, trismus, opisthotonos |
| Botulinum toxin | *C. botulinum* | Blocks acetylcholine release | Descending flaccid paralysis |
| Alpha toxin (lecithinase) | *C. perfringens* | Destroys membranes | Gas gangrene |
| TSST-1, pyrogenic exotoxins | *S. aureus*, *S. pyogenes* | Superantigens | Toxic shock, scarlet fever |
| Endotoxin (lipid A of LPS) | Gram-negative bacteria | TLR4 on macrophages, TNF, IL-1, nitric oxide | Fever, septic shock, DIC |
- Septic shock from Gram-negative pneumonia is distributive: cytokines and nitric oxide dilate arterioles, so systemic vascular resistance falls while heart rate and cardiac output rise (warm shock) until late.
- Diphtheria antitoxin neutralises only toxin that has not yet entered cells, so give it on clinical suspicion. The Elek test (immunodiffusion with antitoxin) shows whether an isolate makes toxin.
Enteric fever (typhoid)
- *Salmonella* Typhi: humans the only reservoir; faecal–oral. Bacteria cross the gut through Peyer's patches, multiply inside macrophages, then after bacteraemia settle in the reticuloendothelial system (liver, spleen, bone marrow) and the gallbladder, which seeds the bowel again and harbours chronic carriers.
- Step-ladder fever, relative bradycardia, rose spots, splenomegaly, leucopenia.
- Blood culture is best in the first week; bone marrow culture is the most sensitive overall; stool and urine positive later. Widal is unreliable.
- Third-week complications: ileal perforation and bleeding from ulcerated Peyer's patches (ulcers run along the long axis of the bowel).
- XDR typhoid (Sindh, 2016): resistant to first-line drugs, fluoroquinolones and ceftriaxone; treat with azithromycin (uncomplicated) or meropenem.
- Vaccines: the injectable polysaccharide vaccine and the typhoid conjugate vaccine (now in Pakistan's schedule) both use the Vi capsular antigen. Widal tests the O (somatic) and H (flagellar) antigens.
Cholera and oral rehydration
- *Vibrio cholerae* O1 or O139: comma-shaped, darting motility, alkaline TCBS agar.
- ORS works because cholera toxin leaves the sodium–glucose cotransporter (SGLT1) untouched: glucose carries sodium into the enterocyte and water follows osmotically. ORS replaces losses; it does not reduce stool volume. Severe cases need IV Ringer's lactate; doxycycline or azithromycin shortens illness.
Meningitis
| Age | Organisms | Empirical treatment |
|---|---|---|
| Neonate | Group B streptococcus, *E. coli*, Listeria | Cefotaxime plus amoxicillin |
| Child and adult | *S. pneumoniae*, *N. meningitidis*, (Hib) | Ceftriaxone |
| Over 50–60, pregnant, immunosuppressed | Pneumococcus, meningococcus, Listeria | Ceftriaxone plus amoxicillin |
- Listeria is a small Gram-positive rod with tumbling motility at room temperature; it grows in the cold and spreads by soft cheese and deli meat; it infects pregnant women and the fetus. Cephalosporins do not cover Listeria (or enterococci), so amoxicillin or ampicillin is first-line.
- Signs of meningeal irritation: neck stiffness; Kernig sign (hip flexed to 90°, knee extension painful); Brudzinski sign. Their absence does not exclude meningitis.
- Suspected meningococcal disease with a non-blanching rash: benzylpenicillin or ceftriaxone at once, before transfer. Waterhouse–Friderichsen syndrome is adrenal haemorrhage with shock.
- *N. meningitidis* ferments glucose and maltose; *N. gonorrhoeae* ferments glucose only. Close contacts get single-dose ciprofloxacin (or rifampicin) to clear nasopharyngeal carriage.
- Pneumococcal meningitis: ceftriaxone (add vancomycin for resistant strains) and dexamethasone, which reduces sensorineural deafness, the commonest sequel (inflammation spreads to the cochlea).
| CSF | Bacterial | Viral | Tuberculous |
|---|---|---|---|
| Cells | Neutrophils | Lymphocytes | Lymphocytes |
| Protein | High | Normal or mild rise | Very high |
| Glucose | Low | Normal | Low |
Pneumonia
- *S. pneumoniae*: commonest community-acquired cause; lancet-shaped Gram-positive diplococci, alpha-haemolytic, optochin sensitive; type-specific antiserum makes the capsule swell (Quellung reaction). Amoxicillin is the usual first choice for mild community pneumonia.
| Stage of lobar pneumonia | Timing | Appearance |
|---|---|---|
| Congestion | Day 1–2 | Heavy, red, boggy; bacteria-rich oedema fluid |
| Red hepatisation | Day 2–4 | Firm, liver-like red lobe; alveoli packed with neutrophils, red cells and fibrin |
| Grey hepatisation | Day 4–8 | Dry, grey-brown; red cells break down, fibrinopurulent exudate remains |
| Resolution | After day 8 | Enzymes digest the exudate; architecture restored (organisation if not cleared) |
- *S. aureus*: after influenza, which destroys ciliated epithelium; cavities, pneumatoceles, haemoptysis.
- Klebsiella: alcoholics and diabetics; upper lobe cavity with fluid level, red-brown currant-jelly sputum.
- Hospital-acquired pneumonia: Gram-negative rods (Pseudomonas, Klebsiella) and *S. aureus*. Cystic fibrosis: *S. aureus* early, *Pseudomonas aeruginosa* the main cause of death later (*Burkholderia cepacia* is ominous).
- Melioidosis (*Burkholderia pseudomallei*): diabetic rice farmers after floods; pneumonia with liver and spleen abscesses; Gram-negative rod with "safety-pin" bipolar staining; fails standard pneumonia antibiotics; treat with meropenem or ceftazidime, then co-trimoxazole; may reactivate years later.
- Lemierre syndrome (*Fusobacterium necrophorum*, an anaerobe): sore throat, then internal jugular vein thrombophlebitis and septic emboli causing cavitating lung nodules.
Infective endocarditis
| Setting | Usual organism |
|---|---|
| Damaged native valve, dental work (subacute) | Viridans streptococci (commonest cause of subacute endocarditis) |
| IV drug user, tricuspid valve, acute | *S. aureus* (flucloxacillin; vancomycin if MRSA) |
| Prosthetic valve, early | *S. epidermidis* |
| Elderly after urinary catheter or bowel procedure | *Enterococcus faecalis* |
| Colon cancer clue | *Streptococcus gallolyticus* (bovis) |
- *Enterococcus* grows in 6.5% salt and bile, hydrolyses aesculin and is intrinsically resistant to cephalosporins; treat with amoxicillin (with gentamicin or ceftriaxone for synergy in endocarditis).
- Take at least three sets of blood cultures from separate venepunctures before antibiotics in a stable patient; previous antibiotics are the commonest cause of culture-negative endocarditis.
- Peripheral signs: Osler nodes (tender finger-pad nodules) and Roth spots (retinal haemorrhages with pale centres) and glomerulonephritis are immune-complex small-vessel lesions; Janeway lesions (painless palmar macules) and splinter haemorrhages are mainly embolic.
Rheumatic fever
- Follows group A streptococcal pharyngitis (not skin infection) after 2–4 weeks; antibodies to M protein cross-react with cardiac myosin and valve tissue (molecular mimicry, type II hypersensitivity). Post-streptococcal glomerulonephritis follows throat or skin infection.
- Pathology: pancarditis; Aschoff bodies (fibrinoid necrosis surrounded by lymphocytes and Anitschkow cells, large macrophages with "caterpillar" or owl-eye nuclei). Acute death is from carditis with heart failure; later, mitral stenosis.
- Primary prevention: treat streptococcal sore throat with penicillin. Secondary prevention: benzathine penicillin IM every 3–4 weeks for years (to age 21 or 10 years after the last attack, longer with carditis).
Other infections FCPS likes
- Tetanus prophylaxis for a dirty, tetanus-prone wound: clean and debride. Full primary course but last dose over 5–10 years ago: toxoid booster only. Incomplete or unknown vaccination: toxoid plus human tetanus immunoglobulin.
- Syphilis: painless, clean-based chancre with a firm edge; spirochaetes on dark-field microscopy; serology may still be negative. Treat early syphilis with one IM dose of benzathine penicillin.
- Spontaneous bacterial peritonitis: ascitic neutrophils over 250/mm³ in cirrhosis; IV cefotaxime or ceftriaxone plus albumin (protects the kidneys); inoculate ascites into blood culture bottles at the bedside.
- Whipple disease (*Tropheryma whipplei*): arthritis (often years earlier), steatorrhoea, weight loss, pigmentation; PAS-positive foamy macrophages in the lamina propria.
- Brucellosis: unpasteurised milk, livestock; undulant fever, sacroiliitis, orchitis; doxycycline with rifampicin or streptomycin.
- *Helicobacter pylori*: urease positive; peptic ulcer, gastric cancer, MALT lymphoma.
Remember Name the bug, then ask how it harms (toxin or invasion), where it hides, and what kills it.
Exam trap Ceftriaxone misses Listeria and enterococci: add amoxicillin in neonates, the elderly and pregnancy.
Exam trap Osler nodes and Roth spots are immune-complex lesions; Janeway lesions are embolic. Tetanus is spastic, botulism flaccid.
How FCPS asks about this
- Subacute endocarditis after dental extraction: viridans streptococci; three blood cultures first.
- Typhoid: blood culture in week one; organisms persist in gallbladder; vaccine uses Vi antigen; XDR treated with azithromycin or meropenem.
- ORS in cholera: sodium–glucose cotransport is intact.
- Meningitis over 50 or pregnant: add amoxicillin for Listeria; contacts of meningococcal disease get ciprofloxacin.
- Lobar pneumonia stages: red hepatisation (neutrophils, red cells, fibrin) then grey hepatisation.
- Rheumatic fever: Aschoff bodies with Anitschkow cells; benzathine penicillin for secondary prevention.
- Diphtheria: toxin ADP-ribosylates EF-2; Elek test for toxigenicity; give antitoxin early.
Test yourself on this topic
5 of the 86 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A healthy 19-year-old had a sore throat a week ago. He now has high fever, tender swelling along the side of the neck and pleuritic chest pain. CT shows thrombosis of the internal jugular vein and multiple cavitating lung nodules. Which organism is most likely?
Answer: Fusobacterium necrophorum
Lemierre syndrome is septic thrombophlebitis of the internal jugular vein after a pharyngeal infection (sometimes peritonsillar abscess or dental infection), typically in previously healthy adolescents and young adults. The usual cause is Fusobacterium necrophorum, an anaerobic Gram-negative rod that is part of the oral flora. Infection spreads into the parapharyngeal space and the neighbouring internal jugular vein, the infected thrombus sheds septic emboli, especially to the lungs (cavitating nodules, empyema), and occasionally to joints and liver. Treatment is prolonged antibiotics with anaerobic cover (a penicillin with a β-lactamase inhibitor, or metronidazole with a cephalosporin), plus drainage of collections.
Lemierre syndrome
- After pharyngitis in a young adult
- Internal jugular vein septic thrombophlebitis
- Septic lung emboli: cavitating nodules
- Organism: Fusobacterium necrophorum (anaerobe)
- Long antibiotics with anaerobic cover
Remember Sore throat, swollen neck vein, spots in the lungs.
Exam trap Remember the anaerobe: standard throat-infection antibiotics may not cover it adequately.
Why the other options are wrong
- Streptococcus pyogenes Group A streptococcus causes pharyngitis and quinsy, but internal jugular septic thrombophlebitis with lung emboli is classically fusobacterial.
- Epstein–Barr virus EBV causes glandular fever, not septic thrombophlebitis.
- Staphylococcus aureus S. aureus causes septic emboli, mostly from right-sided endocarditis.
- Corynebacterium diphtheriae Diphtheria causes a pseudomembrane and myocarditis.
In untreated lobar pneumococcal pneumonia, which stage follows red hepatisation, with a dry grey-brown cut surface as red cells break down and fibrinopurulent exudate fills the alveoli?
Answer: Grey hepatisation
Lobar pneumonia passes through four classic stages. After the early congestion and the red hepatisation (alveoli packed with red cells, neutrophils and fibrin), red cells lyse and the lobe becomes dry and grey-brown: grey hepatisation. Then enzymatic digestion of the exudate allows resolution, usually with full recovery of lung structure. Organisation into fibrous tissue is an abnormal outcome.
Lobar pneumonia stages
- Congestion
- Red hepatisation
- Grey hepatisation
- Resolution
Remember Red then grey, then it clears.
Exam trap Organisation, not resolution, follows if the exudate is not cleared.
Why the other options are wrong
- Resolution Comes after grey hepatisation.
- Congestion The first stage, before red hepatisation.
- Organisation An abnormal outcome, not the usual next stage.
- Caseation Not a stage of lobar pneumonia.
A child dies of an unrelated cause during an attack of acute rheumatic fever. At autopsy the heart shows small nodules in the myocardium with central fibrinoid necrosis, large macrophages with owl-eye nuclei and lymphocytes. What are these lesions?
Answer: Aschoff bodies
Aschoff bodies are the pathological hallmark of rheumatic carditis. They are areas of fibrinoid necrosis surrounded by lymphocytes, plasma cells and large activated macrophages called Anitschkow cells, some of which become multinucleate Aschoff giant cells. They are found in all three layers of the heart. The valve damage that follows leads to chronic rheumatic heart disease.
Aschoff body
- Hallmark of rheumatic carditis
- Central fibrinoid necrosis
- Anitschkow macrophages (owl-eye)
- Leads to valve disease
Remember Aschoff body means rheumatic heart.
Exam trap Owl-eye nuclei here are Anitschkow cells, not CMV inclusions.
Why the other options are wrong
- Gumma A granuloma of tertiary syphilis.
- Rheumatoid nodules Seen in rheumatoid arthritis, not rheumatic fever.
- Caseating granulomas Suggests tuberculosis.
- Libman-Sacks vegetations Sterile valve vegetations of lupus.
Pakistan was the first country to introduce typhoid conjugate vaccine into its routine immunisation programme. What prompted this?
Answer: XDR typhoid outbreak in Sindh
From 2016 an outbreak of XDR typhoid (resistant to chloramphenicol, ampicillin, co-trimoxazole, fluoroquinolones and third-generation cephalosporins; sensitive to azithromycin and carbapenems) spread from Hyderabad and Karachi. Pakistan responded with a typhoid conjugate vaccine (Vi polysaccharide conjugated to tetanus toxoid) campaign and introduced TCV into routine EPI at 9 months in 2019. Unlike the plain Vi polysaccharide vaccine, the conjugate works in infants and gives longer-lasting immunity. Safe water and sanitation remain essential.
Typhoid in Pakistan
- XDR typhoid outbreak from Sindh (2016)
- Sensitive: azithromycin, carbapenems
- Typhoid conjugate vaccine in EPI at 9 months (2019)
- Also: safe water, sanitation
Remember XDR typhoid led to TCV in the schedule.
Why the other options are wrong
- Typhoid eradicated elsewhere Typhoid is not eradicated.
- A polio outbreak Not related.
- Rising hepatitis E cases Not related.
- Tetracycline-resistant cholera Not related.
A man with subacute infective endocarditis has tender nodules on his finger pads and small retinal haemorrhages with pale centres. What is the mechanism of these peripheral signs?
Answer: Immune complex small-vessel damage
Subacute endocarditis causes a chronic antigen load and circulating immune complexes. These deposit in small vessels and cause an immune vasculitis, producing tender Osler nodes on the finger pads and Roth spots in the retina. In contrast, Janeway lesions are painless and thought to be small septic emboli. Both reflect long-standing infection and prompt a search for vegetations.
Endocarditis signs
- Chronic immune complexes
- Tender Osler nodes, Roth spots
- Janeway lesions: painless emboli
- Prompt a search for vegetations
Remember Osler nodes Ouch; Janeway lesions don't.
Exam trap Tender finger-pad nodules are immune, not embolic.
Why the other options are wrong
- Septic emboli lodging in arterioles That explains painless Janeway lesions, not tender Osler nodes.
- Direct bacterial invasion of the skin The organisms are on the valve, not the skin.
- Platelet consumption and bleeding Platelet count is usually adequate.
- Deficiency of vitamin C Not the cause of these signs.
Where this sits in the CPSP syllabus
- Medicine & Allied, Paper 2: Infectious diseases, Bacterial infections of medical importance: typhoid, cholera, meningitis, pneumonia
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