4.12 Rheumatic Fever, Poststreptococcal Disease, Enteric & Hepatic Infections

1. Acute Rheumatic Fever

An immune-mediated sequela of group A streptococcal pharyngitis — not of skin infection — appearing two to four weeks after the sore throat, driven by molecular mimicry between streptococcal M protein and host tissue.

Jones criteria require evidence of preceding streptococcal infection plus two major criteria, or one major and two minor.

Major criteria (mnemonic JONES):

Minor criteria: fever, arthralgia, elevated erythrocyte sedimentation rate or C-reactive protein, prolonged PR interval.

Evidence of preceding infection — elevated or rising antistreptolysin O or anti-DNase B titer, positive throat culture, or positive rapid antigen test — is required. The throat culture is often negative by the time rheumatic fever appears, so serology carries the diagnosis.

Management:

• Anti-inflammatory therapy — high-dose aspirin or NSAIDs for arthritis; corticosteroids for severe carditis.
• Penicillin to eradicate residual organisms, even if the culture is negative.
• Secondary prophylaxis with long-acting intramuscular penicillin G benzathine — this is the highest-yield management point. Duration depends on whether carditis occurred and whether residual valve disease persists, extending for years and sometimes for life.

The long-term consequence is rheumatic mitral stenosis, appearing decades later.

2. Poststreptococcal Glomerulonephritis

A separate blueprint subsection, and the contrasts with rheumatic fever are exactly what the exam tests.

Presentation is a nephritic syndrome: hematuria with dysmorphic red cells and red cell casts, sub-nephrotic proteinuria, edema, hypertension and a rise in creatinine.

Low C3 with a normal C4 is the classic serologic signature, and C3 normalizes within 6 to 8 weeks — persistent hypocomplementemia beyond that window should prompt reconsideration of membranoproliferative glomerulonephritis or C3 glomerulopathy. Management is supportive: salt restriction, diuretics and blood pressure control.

The key teaching point — antibiotic treatment of the antecedent streptococcal infection prevents rheumatic fever but does not prevent glomerulonephritis. This is frequently tested as a direct contrast.

3. Enteric Infections

The blueprint lists enteric infections with subtopics: infectious esophagitis, gastroenteritis, pancreatic infection and abscess, bacterial peritonitis, and intra-abdominal abscess other than liver or pancreas.

Spontaneous bacterial peritonitis

Infection of pre-existing ascites without a surgically treatable intra-abdominal source.

• Diagnosis: ascitic polymorphonuclear count of 250 cells per microliter or more. Treat on this basis; do not wait for culture, which is negative in a substantial minority.
• Usually monomicrobial, typically Escherichia coli, Klebsiella or Streptococcus pneumoniae.
• Treatment: third-generation cephalosporin, plus intravenous albumin on days 1 and 3 in those with renal dysfunction or high bilirubin — albumin reduces hepatorenal syndrome and mortality.
• Secondary prophylaxis after an episode, and primary prophylaxis in low-ascitic-protein or variceal-bleeding patients.

Secondary bacterial peritonitis

Caused by a perforated viscus and requiring surgery, not antibiotics alone. Distinguish it from spontaneous peritonitis using Runyon criteria on the ascitic fluid: polymicrobial culture, total protein above 1 g/dL, glucose below 50 mg/dL, and lactate dehydrogenase above the serum upper limit. Missing this distinction and managing a perforation medically is a classic exam trap.

Intra-abdominal abscess

Suspect it in persistent fever with leukocytosis after abdominal surgery, diverticulitis, appendicitis or perforation. Source control is the treatment — percutaneous or surgical drainage — with antibiotics as an adjunct. Antibiotics alone rarely sterilize an undrained collection.

4. Hepatic Infections

A named blueprint subsection listing viral hepatitis, liver abscess, cholecystitis and cholangitis.

Pyogenic versus amebic liver abscess

The management contrast is the exam point: amebic abscess responds to medical therapy alone and does not routinely require drainage, whereas pyogenic abscess almost always requires drainage. Aspiration of an amebic abscess is reserved for large left-lobe lesions at risk of rupture into the pericardium, diagnostic uncertainty, or failure to respond.

Klebsiella pneumoniae invasive syndrome — a hypervirulent strain causing liver abscess with metastatic infection to the eye (endophthalmitis) and central nervous system — is particularly associated with diabetes and East Asian origin, and warrants a careful ophthalmologic examination.

Acute cholangitis

Charcot triad — fever, jaundice, right upper quadrant pain. Adding hypotension and mental status change gives Reynolds pentad, which indicates suppurative cholangitis. Treatment is antibiotics plus urgent biliary decompression by endoscopic retrograde cholangiopancreatography; antibiotics alone are inadequate when the duct is obstructed, because the infected bile is under pressure.