Chapter 2: Great mimics

It was in the 1960s when I first met the one truly ‘mad’ person that I encountered in my medical career. I had just commenced a short rotation as a psychiatric RMO at a reputable Melbourne psychiatric hospital. The patient was a 52-year-old Londoner who had migrated to Australia with her husband and son. She had been ‘certified’ to the hospital with the presumptive diagnosis of ‘mania—for management’! Taking a history was difficult as she was forever restless, distracted and had flights of ideas. Furthermore she had an alluring ‘fetching’ body language which led to sexual escapades in the hospital grounds with the inevitable willing male inmates. She was soon accommodated in a secure ward and was assessed by the medical director and a consultant neurologist—two extremely brilliant clinicians.

As they left the ward they said, ‘John, we want you to perform a lumbar puncture—we suspect neurosyphilis’. This came as a surprise in view of her apparent clean-cut background and pleasant, doting family members. However, we did determine that she had probably had sexual encounters with servicemen who lived in the family boarding house during World War II.

Well, my futile attempt at performing the procedure was a nightmare which remains with me to this day. The shrieking and wailing (I kept thinking that a banshee would sound like her) were punctuated by threats to the nurse and to me of injury from the instruments we were handling. I was honestly frightened by this unfortunate woman and felt so sad that a human being could be so tormented and manic.

The boss was not impressed with my failure but I heard that the specialist team’s effort to get the cerebrospinal fluid under general anaesthesia was like a scene from Dante’s ‘Inferno’. The spinal fluid did test positive for syphilis.

She was treated with parenteral penicillin and large doses of antipsychotics but unfortunately I have no information about the eventual outcome.

The patient was a 71-year-old male, a native of Papua New Guinea, resident in Australia for six years. He presented with fever, diffuse crackles in the chest and monocytosis.

He was a new patient for me, although the family was well known. Here was a hard-line case who despised doctors because ‘they nearly killed him in hospital some years ago when he had double pneumonia’. He was neither hostile nor enthusiastic—just terribly ill and resigned to the coercion of his family.

On examination he was in a cold sweat and was pale, with a feeble but regular pulse, and rattles all over the chest (back and front). He and his family hammered the previous history of double pneumonia and, to my eternal discredit, I let them divert my proper thinking. His blood count showed a monocytosis of 12 per cent = 972 absolute. Hypnotised by the pneumonia story, I thought of endocarditis complications and gave him amoxycillin. He refused to go to hospital and went home.

Next day he returned, even worse but still refusing to go to hospital. At the risk of overservicing, I did another blood count. The monocytosis had risen to 16 per cent = 1072 absolute. By now, after a good night’s rest, I had shed the shackles of the double pneumonia and was back to normal thinking.

Pallor + cold sweats + shivering + monocytosis + Papua New Guinea = malaria?

Monocytosis is the only consistent abnormality in the malarial blood picture. Long ago, before Field’s stain, monocytosis plus the classical symptoms in the slide-negative case were considered diagnostic. I did Field and thin films: both negative.

Old timers also taught that if large lymphocytes are well in excess of small ones in slide-negative cases, with a long past history and suggestive symptoms, the patient most probably is malarial. The ratio here, large to small, was 22 to 15. Jackpot.

As this author suffers from precisely these same rigors and so on, even 11 years after emigrating from the endemic area, the lucky patient was supplied with combined sulphadoxine and pyrimethamine plus quinine bihydrochloride from personal stock. He trotted in the next day, asymptomatic and doctor-oriented.

Before World War II Britain was dotted with infectious disease hospitals—dubbed ‘fever hospitals’. Scarlet fever, diphtheria, rheumatic fever, chicken pox, whooping cough and measles were rife and often fatal. After the end of the war in 1945, the incidence and severity of the infectious diseases declined dramatically. This was due to the introduction of immunisation programs, a fall in the virulence of the streptococcus, improvement of living standards and the discovery of antibiotics. At the same time, the incidence of tuberculosis increased. Consequently, the emptying infectious disease hospitals became TB hospitals, with wards full of seriously affected children, adolescents and adults. Along came triple therapy—streptomycin, para-amino salicylic acid (PAS) and isoniazid—and the tubercle bacillus was conquered. Hospitals once more began to empty. A similar pattern occurred in Australia: tubercle was dead, or at least thought to be no longer a problem.

THE CASE OF MR HB

Now in his mid-70s, always dapper and very correct, Mr HB had spent the last third of the year suffering from severe sciatica with all its associated pain, analgesics and detailed investigation. Two weeks before Christmas he presented with a unilateral headache. Always a migraine sufferer, he assumed this was one of his usual attacks brought on by the persistent sciatic stress that had disallowed him the normal relaxations in his beloved garden. The story, however, did not quite ring the vasospastic bell and, sure enough, one week later the telltale blebs of herpes zoster of the ophthalmic branch of the right trigeminal nerve began to appear. As he seemed otherwise well, I had no hesitation in prescribing corticosteroids. The nasociliary branch, and therefore the eye itself, remained unaffected, and so we soldiered on through the various stages of the eruption and its attendant pain.

In March, the sciatica began to get really bad again and Mr HB also complained of a persistent dry cough. He remained well. Within the next two months he was assessed by the orthopaedic specialist, and spinal stenosis with the possibility of laminectomy was discussed. The cough had persisted. Despite the absence of clinical signs, I felt it wise to have his chest X-rayed. The report read:

There had been no weight loss, no night sweats, no shortness of breath and no loss of energy.

‘I never told you that I was turned down for military service in 1939’, said Mr HB. ‘They said I had signs of TB. I was most upset. I had never had any trouble before and have had none since.’

I referred him to our thoracic physician who phoned me later. ‘When I bronchoscoped him, his bronchus was full of caseous-looking material, almost completely blocked at the right bronchus.’ Mr HB was admitted to hospital. Infection with the tubercle bacillus was confirmed, and his family went through the usual surveillance. Triple therapy ‘nouveau’ was commenced, and Mr HB was doing very nicely after only seven days.

Milly presented as a dishevelled pensioner with vague undifferentiated chest pain for which she had consulted a variety of health professionals. Although the pain seemed mild, a thorough insight into her lifestyle revealed it was a major disability, and later led to her death.

The first encounter

I vividly remember my first consultation at the end of a busy Saturday morning with Milly, a rather typical 62-year-old Queenslander. Her diminutive figure was crowned with an unruly shock of hair and I felt she was yet another person losing interest in herself and living.

Milly’s presenting complaint was a peculiar type of chest pain: her chest became stiff and sore after activity. She had suffered with it a long time, had tried a variety of medications and had consulted a number of general practitioners without success.

Despite my lack of enthusiasm I took a detailed history. The problem seemed simple, the provisional diagnosis being a musculoskeletal disorder of the chest wall with angina as the differential diagnosis. After checking her blood pressure I prescribed medication and reassured her, arranging for a consultation soon after when I would have blood tests done. On review she claimed to be free of the pain and requested permission to participate in a lawn bowls pennant competition later in the week. Surprised, I agreed.

The merry-go-round

Milly consulted me four weeks later when she admitted the pain was so severe that she had sought the aid of a chiropractor and a physiotherapist. The pain had persisted and she consulted another doctor who referred her to an orthopaedic specialist. She was returning to my care because I had given her the most relief. At each consultation she impressed me as a tired, depressed and lonely pensioner.

Milly presented four months later with severe chest pain. Cardiac enzyme studies were consistent with recent myocardial infarction, confirmed by electrocardiogram (ECG), which also revealed a left bundle branch block.

The home visit—the ‘real’ patient

Milly’s small home was immaculate. It was clean and fresh inside and outside. The carefully manicured garden was a picture. Everything had the mark of a houseproud perfectionist.

I took renewed interest in her with the realisation that the tired little lady I had been seeing in the surgery was not the ‘real’ Milly. It became obvious that the mild chest pain was a major disabling problem. She was unable to bowl as usual, nor was she able to participate in her beloved ballroom dancing. Colleagues at her bowling club gave a new picture of Milly. She was a tireless worker, extremely active and always neat and tidy, but her friends had noticed a recent lack of interest in her appearance.

Managing her angina was difficult but possible with judicious juggling of drugs. I advised Milly that angiography with a view to coronary artery bypass surgery was appropriate. She flatly refused and expressed her greatest fear: some complication would force her to become an inpatient in a nursing home or hospital where she could not pursue full community life. I continued to manage Milly conservatively.

Milly resumed ballroom dancing, albeit with less vigour, and won the State Singles Lawn Bowls Championship for the second time in three years, giving her a feeling of joy and self-worth.

The final home visit

One month after the bowling triumph I was called to her home after the Saturday evening dance. She had classic symptoms of angina, rapidly relieved by standard medication. She settled and rested.

The phone rang early Sunday morning and I sensed something was seriously wrong. At her home I found her dead in bed, having died apparently quietly and peacefully in her sleep.

John R, a 50-year-old accountant, was an avid ballroom dancer and tennis player, but his activity was curtailed by persistent low-back pain and right-leg pain. Pain in his back and right buttock would radiate into his thigh and calf after only five minutes of dancing or tennis.

He was referred to me for an epidural injection to alleviate his back pain and sciatica. An accompanying X-ray confirmed degeneration of his L5–S1 intervertebral disc. Examination of his lumbosacral spine revealed tenderness at this level and restricted flexion and extension movements. At follow-up four weeks later, he claimed that the injection had not helped.

DIAGNOSIS AND OUTCOME

The ‘penny dropped’ when I reflected on the nature of the pain. Despite his relative youth he obviously had vascular claudication. He was a moderate smoker. In addition, he claimed his erections were ‘not as good as they should be’.

Following exercise, auscultation revealed a loud bruit over the aortic bifurcation, the right common iliac artery and the right femoral artery. The peripheral pulses were weaker in his right leg. I referred him to a vascular surgeon who ordered an angiogram (Figure 2.1), which confirmed arterial disease including a tight stenosis in his right common iliac artery and the left internal iliac with an aneurysm in the distal part of the left common iliac artery. John underwent aorta bi-iliac dacron grafting (Figure 2.2) and for the past eighteen years has been untroubled by leg pain, although he has suffered a myocardial infarction.

MRS GULLIVER

Mrs Gulliver, a widow who had just had her 50th birthday, was always smartly dressed and neatly coiffured, and she presented well. Fay, her only child, was 13 years old. Mrs Gulliver sat straight before me, head forward, shiny eyes staring straight into mine. ‘You must tell me the absolute truth, Doctor.’

The absolute truth in the report on my desk was most unkind: ‘The mediastinum is enlarged and there is presence of a mass in the superior and anterior mediastinum … I would consider in particular bronchogenic neoplasm.’ I thought of her 30 cigarettes a day for 20 years. I also thought of the small supraclavicular lymph nodes seen by one of my partners about a year ago and the dysphagia (barium swallow negative) complained of six months before.

Mrs Gulliver had presented two months ago complaining of morning stiffness and pain affecting neck, trapezius and deltoid muscles. She was extremely tender and the pain made her miserable. She had had a previous rotator cuff problem. ‘This is different’, she declared. Erythrocyte sedimentation rate (ESR) was 65, white cell count (WCC) 12 000, and my heart leapt at the magic response to prednisone. But every time I tried to reduce the dose, the pain and stiffness recurred. She latterly complained of a persistent cough and full feeling in the middle of the chest; thus the disastrous chest X-ray.

MR FREDERICKS

Mr Fredericks, an 80-year-old, had developed during his past 10 years a potpourri of pathology—tic douloureux, atrial fibrillation with congestive cardiac failure, severe diverticular disease, and the expected degenerative disease of cervical spine and shoulder joints. His main complaint became severe pain affecting neck and shoulder girdle and hips, worse in the night and early morning, with associated stiffness. He did not respond to physiotherapy or anti-inflammatory medication. A full blood examination showed an ESR of 57 mL/h. A presumptive diagnosis of polymyalgia rheumatica was made and a therapeutic trial of prednisone commenced. The improvement was definite and dramatic and allowed him to return to his physical work on a somewhat large piece of land. This improvement continued, if less positively, over a period of six months until he asked for a home visit because of the severe intractable pain affecting neck, shoulders and upper back.

He was referred for an opinion:

Orchidectomy and radiotherapy induced pain relief and for some months at least he was able to return to normal activities. How are the mighty fallen.

Jack, aged 15 months, was brought by his parents because of increasing diarrhoea with six large offensive stools daily. He had been seen by another doctor four weeks earlier who considered an infective cause but stool microscopy and culture showed no parasites and no growth of pathogens. A trial of tinidazole seemed to aggravate the diarrhoea. He was unwell, anorexic, miserable and irritable, had abdominal bloating and lost weight. Jack seemed to thrive when breast fed for 10 months and only started eating solid food four months ago. He was diagnosed as having coeliac disease.

Siobhan, aged 32 years, presented with several days of malaise, lethargy and mouth ulcers. Over the past 10 months she had suffered from flatulence and bloating in addition to loose bowel actions about three times a day interspersed with short periods of constipation. She described ongoing fatigue and weight loss of 8 kg over this time. On examination she was a pale, thin, tall woman with no subcutaneous fat. Diagnosis: coeliac disease.

Cathy, aged 46, gave this testimony to our local newspaper: ‘My coeliac disease was picked up by accident as I was asymptomatic. It started two years before that when my teenage daughter was quite sick, always complaining of tummy pains and being tired. We went to seven specialists in 18 months. They looked at everything and finally tested for coeliac disease. Her blood tests were sky-high so the family had to be tested and I came back positive. I had a biopsy which gave the positive diagnosis. Being diagnosed has been the best thing as we’ve got a totally new lease on life’.

Roger G, aged 66, was a retired retail manager who presented with several days of dull pleuritic chest pain radiating to the left side of the chest.

He had a history of a myocardial infarction 20 years previously and recent transient ischaemia attacks for which he had been prescribed warfarin. This treatment was suspended following a bleeding duodenal ulcer. He responded well to H2 receptor antagonist therapy. He also suffered from insulin-dependent diabetes and glaucoma.

Examination revealed evidence only of chronic obstructive airway disease. This clinical diagnosis was confirmed on a chest X-ray, which also showed a slightly enlarged heart shadow and an unfolding of the aorta. Other tests included cardiac enzymes, which were normal, and a full blood count, which showed Hb 11.0 g/dL, WCC 4100, platelets 187 000, Na 137 mmol/L, K 4.0 mmol/L, Cl 81 mmol/L, Ca 2.35 mmol/L. Urinalysis was clear.

An electrocardiogram showed an old inferior infarction and normal sinus rhythm but no recent changes. A diagnosis of ‘chest wall syndrome’ was made and the patient was given supportive and symptomatic treatment. However, because the chest pain persisted, and as an infolding of the thoracic aorta was reported on chest X-ray, a CT (computerised tomography) scan of the thorax was ordered and it reported as normal.

Roger was referred to a physician who repeated the chest X-ray. This X-ray showed a crush fracture as well as moderate osteoporosis in the vertebrae.

DIAGNOSIS AND OUTCOME

Roger was admitted to hospital for a series of tests. These included a bone marrow cytological aspirate and a bone scan. The bone marrow biopsy showed plasmacytosis with atypical primitive and multinucleated forms.

The bone scan showed multiple malignant deposits in ribs and in the skull. In particular, there was increased uptake in the left first rib and absent foci of uptake in the inferior pole of the sternum. The CT scan showed changes of myeloma: multiple lytic areas with wedging at T8 and compression of the body of L5 and some destruction of L4.

The diagnosis now was non-secretory multiple myeloma. The chest pain was secondary to myeloma lesions in the thoracic vertebrae.

Roger was treated with regular courses of melphalan and prednisone. His complete blood count was monitored and he received analgesics when required. He died three years after presentation.

Day 1—Tuesday

Miss M W, aged 8, presented with epigastric pains. There were no other symptoms.

She had a low-grade fever, the right iliac fossa was mildly tender and bowel sounds were slightly hyperactive. However, she appeared quite well and had no significant past history.

A tentative diagnosis of early appendicitis or viral mesenteric adenitis was made. There was no reason to consider functional disease high among the diagnostic probabilities. She was discharged to her mother’s care for observation at home and general advice on follow-up was given.

Day 4—Friday morning

M’s pain had been smouldering but there were no new symptoms. She appeared to be well generally and was quite cheerful. The low-grade fever continued: she now had mild tenderness in the right upper quadrant but the liver was impalpable and there was no jaundice. No urine specimen was available for testing; no other physical abnormalities were detected despite an exhaustive examination.

Hepatitis was promoted now to the head of the list of diagnostic probabilities despite a negative history of contact. The mother was asked to check the colour of urine and faeces and was given general advice. No pharmacological action was taken nor had proprietary analgesics been given.

The mother later phoned to say that M’s urine was dark. She was asked to bring in a urine specimen.

Day 4—Friday afternoon

M’s urine was indeed dark and testing was positive—not for bilirubin but for blood; there was no proteinuria. With a working diagnosis of glomerulonephritis, a most searching history was unhelpful and a repeated physical examination still revealed only mild tenderness in the right upper quadrant. She was asked to return with an early morning specimen.

Day 5—Saturday morning

M returned with a urine specimen that was still positive (+ +) for blood but otherwise was normal. An additional symptom now had appeared: her bowel motions that morning were black and tarry. An occult blood test was positive.

The working diagnosis now centred on haemorrhagic diatheses such as Henoch-Schölein or idiopathic thrombocytopenic purpura. However, there was no splenomegaly, no lymphadenopathy, no clinical jaundice, no masses, no rash and no other clinical evidence of haemorrhagic disorder such as bruising or petechiae; heart sounds were dual.

Day 5—Saturday afternoon

An urgent full blood examination, ESR and clotting profile gave a diagnosis. The clotting parameters were marginally impaired, ESR was 10, and the red cell parameters were normal and the white cell count was within normal limits; but a differential count revealed 50 per cent atypical lymphocytes, and serology confirmed a diagnosis of glandular fever. Urine microscopy had confirmed the dipstick finding of haematuria. Even with a diagnosis firmly established no clinical evidence of Epstein-Barr mononucleosis could be found.

On the assumption that her haematuria and melaena reflected impaired hepatic function, M was given 10 mg of vitamin K by intramuscular injection.

Day 6—Sunday

Urine was still weakly positive (trace) for non-haemolysed blood; bowel motions were still dark. Submandibular node enlargement was detected for the first time. The liver and spleen were impalpable and the nodes elsewhere were normal. There was no rash.

Day 8—Tuesday

The submandibular nodes were now unmistakeably enlarged. There was no fever, pharyngitis or rash. Lymph nodes elsewhere were normal. Both the liver and the spleen were enlarged but neither was tender. Urinalysis was normal and the mother reported that bowel motions were now a normal colour and consistency.

M had remained clinically well and cheerful throughout the course of her illness and currently is under a customary conservative management regime. Subsequently she developed the typical purplish rash of infectious (Epstein-Barr) mononucleosis on the lower abdomen.

The history started on a Friday evening. The patient had been unusually quiet on the way down with her husband to their seaside cottage for the weekend and during dinner developed sudden and severe rigors. She had been perfectly well up to this time—a minor non-extractive dental procedure had been performed two to three weeks previously.

Rigors continued intermittently during the next two days. The husband, who was wont to be critical of the fact that many doctors—particularly the younger ones—no longer carried thermometers as part of their home visiting kit, just happened to have one in his pocket. He noted that, while afebrile in the evening, the temperature, coincident with a rigor, reached 41 °C in the early hours of the morning.

On Monday morning the blood picture, including the ESR, was shown to be completely normal. There was no pus in the urine, and an X-ray of the chest was clear apart from calcification of the mitral valve, which an experienced radiologist pointed out was present in the ring and was not involving the cusps. There was no lymphadenopathy, no splenomegaly or liver enlargement, but a pansystolic mitral murmur, known to be present for some years, seemed rougher and louder. The husband referred the patient, fairly sure that he was about to be involved in only the second case of infective endocarditis seen in his medical lifetime.

The physician to whom the patient was referred tended to agree. She developed just palpable splenomegaly, the rigors continued daily, and, apart from the cardiac bruit, no further abnormal physical signs were found. Or rather the husband-doctor did not think so. A capable registrar thought he could hear a mitral diastolic murmur as well as one at the left sternal border, and a cardiologist who came with his echocardiograph demonstrated what he maintained were vegetations on both valves.

The husband, who had been brought up on mere stethoscope diagnosis of valve lesions, was somewhat unconvinced and uncharitably suggested that perhaps some of the green flashes could have been due to a loose wire or something in the machine he had never been quite so close to before. Nevertheless, in spite of repeatedly negative blood cultures—a dozen or so in the first five days—he was importunate enough to press the physician captain of the team to do something, even to the extent of starting intravenous penicillin, long-term commitment though this would mean.

In the meantime blood pictures remained normal, unlikely parasites had been looked for, exotic agglutinations done, and chest X-rays and ECGs remained unchanged.

On the morning of the seventh day the mononuclear cells in the film were declared atypical and foamy, the Paul-Bunnell became positive to a titre of 1/1280, and the rigors ceased. No prodromal illness, no sore throat or pharyngeal exudate, no lymphadenopathy, minimal splenomegaly?

She was, of course, a doctor’s wife.

Adam R, a 23-year-old laboratory technician, presented with a one-week history of a sore throat, headache, fever and lethargy. Examination revealed a temperature of 38.1°C, pharyngitis and cervical lymphadenopathy. I ordered a Paul–Bunnell test and took a throat swab, which produced negative results. I then instructed him to take the penicillin I had prescribed.

He returned in five days saying that he felt worse, and he now had developed a rash. The rash was a fine salmon-pink maculopapular rash on the upper trunk and extremities, and it included the palms of the hand. This made me wonder about secondary syphilis, but I thought it more likely to be a viral exanthema or a drug reaction. In addition enlarged nodes were now palpable in the groin and he had hepatomegaly. I thought that it must be Epstein-Barr mononucleosis and ordered more blood tests.

On review he had developed a painful rash on his face: herpes zoster affecting the ophthalmic division of the 5th cranial nerve.

DIAGNOSIS AND OUTCOME

It was time to consider human immunodeficiency virus (HIV) infection and so I ordered HIV screening tests; these were positive. The process of breaking the news to Adam was the really difficult step. He was referred to a specialist clinic and died two years later.

Josie M, a 21-year-old higher degree student, presented in great distress on the eve of her wedding. She had developed a coarse dark-pink rash over most of her body five days previously and was informed by the young doctor at the university health service that she probably had secondary syphilis: ‘The rash is typical; I’ll start you on penicillin and organise some special blood tests’.

Josie, who came from a very religious family and was known to me as a straight, hard-working, intelligent, attractive girl, was ‘numb with disbelief. Here I am getting married in two days to the only man I have ever loved and I’m told I have syphilis. Can you believe it? Could I have picked it up from a toilet? Surely Peter couldn’t have it—he’s so faithful. Look at me, I have this unsightly rash on the neck and chest and I’m supposed to look beautiful on my wedding day’.

DIAGNOSIS AND OUTCOME

While I was looking at the rash (as Josie wept) and fighting feelings of disbelief at such stupidity from a colleague, I inquired, ‘Did you notice a roundish mark on your skin before the rash appeared all over your body?’

‘Yes—around my tummy. I thought it must have been a ringworm I picked up on the farm.’ Yes, Josie had the common problem of pityriasis rosea. Josie went off happily with appropriate reassurance, advice about make-up for the rash on exposed parts and some undeserved support for my colleague (‘This rash tricks us all the time—I had never heard about it in my medical course but I heard a lot about syphilis’). Josie lived happily ever after (well, for about seven years until she was divorced).

The story of Miss Sue W, an international university student, was brought to my attention when I was asked to prepare a report for medical defence. She presented to the university student health service with three months of coughing, wheezing and dyspnoea on exertion. The problem was diagnosed as bronchial asthma and salbutamol was prescribed. The patient reported back in one week and said that she felt only slightly improved, so a combined corticosteroid and beta agonist inhaler was prescribed. She then reported a significant improvement at first but then she said she developed a cold with a persistent fever and the respiratory symptoms were worse. She was then prescribed a short course of oral corticosteroids.

Eventually Sue was found comatose by her flatmate and was taken to hospital where she was found to have miliary tuberculosis and tuberculoid meningitis. According to her flatmate she gradually deteriorated with weight loss and weakness, became frustrated, confused and irritable and refused to seek medical attention. She still remains in a semi-coma in her home country and requires constant nursing care. The medico-legal consequences were massive.

Another medico-legal case was that of a 25-year-old South African white woman who was visiting Australia on an extended holiday to see relatives. She visited a country practice complaining of coughing and wheezing. She was also treated for bronchial asthma for several weeks before pulmonary tuberculosis was diagnosed on chest X-ray.

The great mimics of the past were the notorious infections: syphilis and tuberculosis. A host of other infections and neurological disorders also represented past mimics. The major diseases of modern Western society, atherosclerosis and malignant disease, have replaced the great infections of the past century as the major life-threatening diseases. Surprisingly, atherosclerosis in its various manifestations of coronary artery disease, cerebrovascular disease and peripheral vascular disease can mimic a number of conditions and the diagnosis can be difficult initially. Malignant disease, especially lymphoma, multiple myeloma and carcinoma of the central nervous system, lungs, kidney, caecum and other internal organs or ‘silent areas’, can mimic a variety of diseases.

The infections, malaria and Epstein-Barr mononucleosis, as represented in this chapter are mimics; and we must not forget tuberculosis and syphilis. Other important mimics include the various endocrine disorders and the rheumatic or connective tissue diseases such as systemic lupus erythematosus, polymyositis and polymyalgia rheumatica.

Now we have HIV infection and we will have to be forever vigilant to make an early diagnosis of this disease and all its protean manifestations.