Infectious Diseases Department

What our infectious diseases unit covers — and who it is for

Infectious diseases is the medical specialty concerned with infection: identifying the organism responsible, choosing the treatment that will reach it, and deciding how long that treatment needs to run. It is also, increasingly, the specialty responsible for the opposite problem — stopping antibiotics that are not helping, because every unnecessary course makes the next infection harder to treat for everybody.

It is an unusually consultative specialty. Most of its patients are already under someone else: the surgeon whose wound is not healing, the haematologist whose patient has a fever, the cardiologist with a murmur and positive blood cultures, the intensivist with an organism nobody recognises. The unit also runs its own clinics for chronic viral infection, tuberculosis, travel medicine and the infections that follow transplantation.

At Acıbadem International the work is organised into five strands.

• Diagnosis of undifferentiated infection — fever with no obvious source, abnormal inflammatory markers, and the organisms that hide in places the first round of tests does not look.
• Treatment of resistant and complicated infection — multidrug-resistant bacteria, deep-seated infection of bone, joint, heart valve and implanted devices, and infection that has failed one or more previous courses.
• Infection in the immunocompromised — patients on chemotherapy, after transplantation, on biologic therapy, and those with fever and a low neutrophil count, where the timescale is measured in hours.
• Chronic viral infection — hepatitis B, hepatitis C and HIV, all three of which have moved from being fatal to being managed conditions within one professional lifetime.
• Travel, vaccination and the diseases of this region — pre-travel advice and immunisation, fever in the returning traveller, and the infections that are common here and rare in the countries most of our patients come from.

Where the borders sit. Infection confined to one organ is often managed by that organ’s specialty with advice from here — pneumonia with pulmonology, urinary infection with urology, skin infection with dermatology. The laboratory that identifies the organism and tests its susceptibility belongs with pathology and clinical microbiology, and the two work as one service. Vaccination before and after solid organ transplantation is planned with organ transplantation.

What an infectious disease doctor actually does

An infectious disease doctor — an infectious disease specialist — is a physician trained in internal medicine who has sub-specialised in infection and, in this country, in clinical microbiology alongside it. The work has three parts, and only one of them is prescribing.

The first is the history, which in this specialty is closer to detective work than anywhere else in medicine. Where have you been, what did you eat, what animals do you keep, what surgery have you had, what is in your body that was not there when you were born, who else is ill, what antibiotics have you already taken, and what were you taking them for. Infections are acquired somewhere, from something, and the exposure usually names the organism before any test does.

The second is interpreting microbiology, which is harder than it looks. A positive culture is not automatically the cause of the illness — it may be a contaminant from the skin, or a colonising organism that lives on a surface without invading it. A negative culture does not exclude infection, particularly after antibiotics have been started. Reading a susceptibility report means knowing which drug reaches which tissue, not simply which box is marked sensitive.

The third is duration and de-escalation. Deciding when to stop is a specific skill, and it is where infectious diseases differs most sharply from the instinct of everyone else involved. Longer is not safer; it is simply longer, with more side effects, more resistance and more damage to the patient’s own bacterial populations.

Fever of unknown origin

Fever of unknown origin describes a fever that has persisted for weeks, has reached a defined temperature repeatedly, and has survived a reasonable set of initial investigations without a diagnosis. The definition matters because it excludes the ordinary: a week of fever is not fever of unknown origin, it is usually a virus.

What is striking about the classical work on this subject is that infection accounts for well under half of it. The differential divides into four groups, and an infectious diseases unit that only looks at the first is the wrong unit for the job.

• Infection — abscesses in places that do not hurt much, particularly intra-abdominal and dental; tuberculosis, especially outside the lung; endocarditis, especially culture-negative; brucellosis; osteomyelitis of the spine.
• Malignancy — lymphoma above all, along with renal cell carcinoma and some leukaemias, all of which can produce weeks of fever before anything is palpable.
• Inflammatory and autoimmune disease — adult-onset Still disease, giant cell arteritis and the vasculitides, and the periodic fever syndromes, which in this region means familial Mediterranean fever more often than anywhere in Europe. That work is shared with rheumatology.
• Everything else — drug fever, which is common and consistently forgotten; venous thromboembolism; thyroiditis; and factitious fever.

The method is repetition rather than escalation. History and examination are repeated, because findings appear over time that were absent at the first visit. Medicines are reviewed, all of them, including the ones the patient does not consider medicines. Imaging is directed rather than universal, and blood cultures are taken off antibiotics wherever that is safe, because cultures taken through treatment are frequently the reason a diagnosis is never made.

A meaningful proportion of these fevers resolve without a diagnosis ever being reached. That is a recognised outcome rather than a failure, and the honest version of the conversation says so early instead of at the end of a fourth CT scan.

Blood cultures, inflammatory markers and what they mean

Almost every decision in this specialty rests on a laboratory result, and the two most-ordered results are the two most misread.

Blood cultures

A blood culture is the single most valuable test in serious infection, and its value depends almost entirely on how it was taken. Volume is the dominant variable — an underfilled bottle is the commonest reason an organism is missed. Two sets from separate sites give a way to tell true infection from skin contamination, since a skin organism appearing in one bottle of one set means something different from the same organism in every bottle of both. Cultures are drawn before antibiotics start wherever the delay is safe.

Some organisms carry their own meaning. Staphylococcus aureus in the blood is never dismissed as contamination and always prompts a search for a deep focus, because it seeds heart valves, bone and prosthetic material. Streptococcus gallolyticus prompts a colonoscopy. Candida in the blood is never a contaminant.

CRP, procalcitonin and the limits of a number

C-reactive protein rises with inflammation of any cause and says nothing about whether that inflammation is infectious. Procalcitonin rises more specifically with bacterial infection and falls quickly as it resolves, which makes it more useful for deciding when to stop antibiotics than for deciding whether to start them. Neither test diagnoses infection, and neither excludes it — a normal marker in an unwell patient is a reason to look harder, not a reason to relax.

Sepsis and septic shock

Sepsis is not a particular infection. It is what happens when the body’s response to any infection begins to damage its own organs — the lungs, the kidneys, the clotting system, the circulation. Septic shock is the subset in which the circulation fails and blood pressure cannot be maintained without drugs, and it carries the highest mortality in acute medicine.

Its clinical features are unhelpfully non-specific: fever or an abnormally low temperature, fast breathing, a fast heart rate, confusion, reduced urine output, mottled skin. In older patients the presentation is often confusion and a fall with no fever at all, and in the immunocompromised the fever may be the only sign there is.

Treatment is a set of things done together and quickly rather than in sequence: cultures taken, broad antibiotics given, fluids started, the source identified and drained or removed, and organ support in intensive care where it is needed. The time to the first dose of an appropriate antibiotic is one of the few variables that changes outcome, and it is the reason sepsis protocols exist in every hospital. Sepsis is a medical emergency and is treated in hospital, immediately, wherever the patient happens to be.

The second half of the job belongs to this unit and happens after the first day: narrowing the antibiotic once the organism is known, finding the source if the first search missed it, and stopping treatment at the right point rather than the comfortable one.

Antibiotic resistance and stewardship

Antibiotic resistance is the defining problem of this specialty and the reason it exists in its modern form. Bacteria acquire resistance through mutation and by exchanging genetic material with each other, and every course of antibiotics — appropriate or not — selects for the organisms that survive it. The consequence is cumulative and shared: resistance acquired in one patient circulates.

Antibiotic stewardship is the organised attempt to slow that. It is often misdescribed as rationing. It is not — it is the discipline of giving the right drug, by the right route, for the right duration, and stopping it when the indication ends. In practice that means four habits: taking cultures before treatment so that narrowing is possible later; starting broad in a severely ill patient and then narrowing deliberately once the organism is known; switching from intravenous to oral as soon as the patient can absorb, which shortens hospital stays and removes line infections; and setting a stop date at the moment of prescribing rather than reviewing indefinitely.

The evidence on duration has moved consistently in one direction for two decades: for a long list of common infections, shorter courses perform as well as longer ones. Where a shorter course is appropriate it is not a lesser treatment, and a patient told to stop at day five rather than day ten has not been short-changed. Which infections those are, and for which patients, is a clinical judgement made by the team treating you — not a rule to apply from a web page, and never a reason to stop a course early on your own.

The resistant organisms, in plain terms

Resistance is usually reported as an acronym, and patients are rarely told what any of them mean. They are worth knowing, because they determine which drugs remain available and where treatment can be given.

ESBL

ESBL stands for extended-spectrum beta-lactamase — an enzyme produced by some strains of Escherichia coli and Klebsiella that destroys most penicillins and cephalosporins. An ESBL-producing organism is not more aggressive than its sensitive relatives; it is simply harder to treat, and it removes the oral options that would otherwise have allowed treatment at home. It is common in urinary infection, spreads through the gut rather than the air, and is carried harmlessly by a large number of healthy people, particularly after travel to regions where it is prevalent. Carriage is not infection and is not treated.

MRSA and VRE

MRSA is Staphylococcus aureus resistant to the standard anti-staphylococcal penicillins, and VRE is enterococcus resistant to vancomycin. Both are frequently carried on skin or in the gut without causing disease. The distinction between colonisation and infection governs everything that follows: a patient colonised with MRSA who needs an operation may need decolonisation beforehand, but does not need treatment for an infection they do not have.

Carbapenem resistance and the resistant Gram-negatives

Carbapenem resistance is the current edge of the problem. Carbapenems are the class held in reserve for the most resistant Gram-negative bacteria, so organisms resistant to them — some Klebsiella strains, Acinetobacter, and the Pseudomonas infection seen in intensive care and in damaged lungs. Treatment depends on newer combination agents and sometimes on drugs abandoned decades ago for their toxicity, and it is always guided by susceptibility testing rather than by pattern. These infections are largely acquired in hospitals and intensive care units, which is why infection prevention — hand hygiene, line care, isolation, environmental cleaning — is part of this unit’s work rather than a separate administrative function.

Fungal infection

Fungal infection covers two very different clinical problems that share a word. Superficial fungal infection of skin, nails and mucous membranes is common, rarely dangerous and usually managed by dermatology. Invasive fungal infection — fungus in the blood, lungs, sinuses or brain — occurs almost exclusively in people whose immune defences are impaired, is difficult to diagnose and is frequently fatal when it is found late. This unit deals with the second.

Candida and invasive candidiasis

Candidemia is Candida in the bloodstream, and it is the commonest invasive fungal infection in hospital. It arises in patients with intravenous lines, recent abdominal surgery, prolonged broad-spectrum antibiotics, or parenteral nutrition — the classical picture is a patient who is not getting better on antibiotics for something else. Invasive candidiasis extends the same problem into the abdomen, heart valves, eyes and bones.

Two management points are consistently missed. Every patient with Candida in the blood needs an eye examination, because the organism seeds the retina and untreated endophthalmitis costs vision. And every intravenous line is removed or exchanged, because the fungus forms a biofilm on plastic that no drug penetrates while the line stays in.

Aspergillosis and mucormycosis

Aspergillus is inhaled by everybody and cleared by everybody with working lungs and neutrophils. In prolonged neutropenia, after stem cell or lung transplantation, or on high-dose corticosteroids, it invades — most often the lung, producing a pattern on CT that is often the first evidence there is. Diagnosis leans on imaging and on antigen testing, because getting a tissue sample from such patients is frequently unsafe.

Mucormycosis is rarer, faster and more destructive, with a strong association with poorly controlled diabetes and diabetic ketoacidosis as well as with haematological malignancy. It invades blood vessels and kills the tissue they supply, classically spreading from the sinuses towards the orbit and brain. It is one of the few infections where surgery is as important as any drug: the dead tissue has to be removed, often more than once, and antifungal treatment alone does not work. The other half of the treatment is correcting what allowed it — the glucose, the acidosis, the immunosuppression.

Neutropenic fever and infection in the immunocompromised

Neutropenic fever is a fever in a patient whose neutrophil count has fallen below a defined threshold, almost always after chemotherapy. It is treated as an emergency for a specific reason: neutrophils produce most of the visible signs of infection, so a patient without them can be overwhelmingly infected while showing almost nothing. There may be no pus, no redness, no consolidation on a chest film — only a temperature. Broad-spectrum antibiotics are started immediately after cultures are taken, before any organism is known, and that sequence is not negotiable.

The subsequent decisions are where this unit earns its place: which patients can be treated orally at home and which cannot, when to add antifungal cover for a fever that persists, and when to stop. Risk-stratification tools exist for the first question, and the answer depends on the expected duration of neutropenia, the presence of organ dysfunction and the practical question of how far the patient lives from a hospital.

Infection after transplantation and on immunosuppression

After a solid organ transplant the infection risk follows a predictable timetable, and knowing it narrows the differential enormously. The first month is dominated by surgical and hospital-acquired infection — the wound, the lines, the urine, the chest. The period from roughly one to six months, when immunosuppression is heaviest, is when the opportunistic organisms appear: cytomegalovirus above all, along with Pneumocystis, fungal infection, and reactivation of tuberculosis or hepatitis B acquired long before. Beyond six months, stable patients drift back towards ordinary community infections, while those still heavily immunosuppressed stay in the opportunistic window.

CMV infection — cytomegalovirus — deserves separate mention because it behaves differently from most infections here: it is usually reactivation of a virus the patient already carried, it is monitored by measuring viral load rather than waiting for symptoms, and it is treated pre-emptively when that load rises. Prophylaxis against it and against Pneumocystis is standard after transplantation, and screening the recipient — and where relevant the donor — before transplantation is what makes the timetable predictable at all.

Biologic therapy has extended this work well beyond transplantation. Anti-TNF agents and other targeted immunosuppressants used in rheumatology, gastroenterology and dermatology reactivate latent tuberculosis and hepatitis B, which is why screening for both before starting them is mandatory rather than cautious.

Tuberculosis

Tuberculosis remains among the leading infectious causes of death worldwide, and it is the disease this specialty is least willing to miss, because it is curable and because the consequences of missing it compound over months.

Latent tuberculosis

Latent tuberculosis is infection without disease: the organism is present and contained by the immune system, the person is well, has a normal chest radiograph and is not infectious to anyone. It is detected by a tuberculin skin test or an interferon-gamma release assay, neither of which distinguishes latent infection from active disease — that distinction is clinical and radiological.

It matters because containment can fail, and the situations in which it fails are known: anti-TNF and other biologic therapy, transplantation, high-dose corticosteroids, HIV, dialysis, and some cancers. Latent tuberculosis treatment is a defined course of one or two drugs taken for months, and it is offered when the risk of reactivation outweighs the risk of the drugs — a calculation that depends on the individual and is made with the doctor who is prescribing the immunosuppression.

Active disease, including outside the lung

Pulmonary tuberculosis presents as a cough lasting weeks, weight loss, night sweats and fever, and is diagnosed on sputum microscopy, molecular testing and culture, with molecular tests now giving both the diagnosis and the first resistance information within hours rather than weeks.

Extrapulmonary tuberculosis is the part that gets missed, and it is a substantial share of cases: lymph node, pleural, bone and spinal, abdominal, genitourinary, and tuberculous meningitis. It presents without a cough, often without fever, and frequently reaches a surgeon or an oncologist before it reaches this unit, because a mass that is slowly enlarging looks like a tumour. Spinal tuberculosis causing back pain over months in someone from an endemic region is one of the classic missed diagnoses in medicine.

Drug resistant tuberculosis — resistance to the two most important first-line drugs, and beyond that to the newer classes — requires longer treatment with more toxic agents and is managed only where the drugs, the monitoring and the expertise are all present. Treatment of any active tuberculosis is a combination of several drugs taken together for months; taking one alone generates resistance, which is why the regimens are fixed and why supervision of adherence is part of the treatment rather than a comment on the patient.

Hepatitis B and hepatitis C

These two viruses have moved further in one professional lifetime than almost anything else in medicine, and public understanding has not caught up with either.

Hepatitis C treatment

Hepatitis C is curable. Direct-acting antiviral therapy taken orally for a matter of weeks clears the virus in the great majority of people treated, including those with cirrhosis and those who failed the interferon-based treatments of the past. There is no injection, the side effects are mild by the standards of what came before, and cure is confirmed by an undetectable viral load some months after the course ends. Hepatitis c treatment is now one of the most effective interventions available in internal medicine, and the main obstacle in most countries is that people do not know they are infected — the infection is silent for decades.

Two things do not change with cure. Cirrhosis already established does not reverse completely, so surveillance for liver cancer continues afterwards. And cure confers no immunity: reinfection is possible where exposure continues.

Hepatitis B treatment

Hepatitis B is different, and the difference is regularly misunderstood by patients who have read about hepatitis C. It is controlled rather than cured. The virus persists in liver cell nuclei in a form current drugs cannot eliminate, so hepatitis b treatment suppresses replication, halts liver damage and reduces the risk of cancer, but is generally long-term and in many cases lifelong.

Not everyone with hepatitis B needs treatment. The decision rests on the phase of infection — viral load, liver enzymes, the degree of fibrosis, and e-antigen status — and some people are monitored for years without any drug, which is a legitimate plan rather than neglect. Two situations do require treatment or prophylaxis regardless of phase: pregnancy with a high viral load, to prevent transmission to the baby, and any course of immunosuppressive or cancer therapy, because reactivation of hepatitis B during chemotherapy can be fatal and is entirely preventable. Screening before immunosuppression is therefore routine.

Hepatitis B is also vaccine-preventable, and household contacts of an infected person are screened and vaccinated. Care is shared with gastroenterology and hepatology.

HIV

HIV is a manageable chronic condition. Modern antiretroviral therapy is usually one tablet a day, suppresses the virus to undetectable levels in most people who take it consistently, and restores life expectancy close to that of the general population. The single most important fact about it is the one that has travelled least: a person on effective treatment with a sustained undetectable viral load does not transmit the virus sexually.

What determines outcome is the timing of diagnosis, not the drugs. Late diagnosis — presenting with an opportunistic infection because the immune system has already been damaged — remains the main driver of illness and death, and it is why testing is offered widely rather than only to people who ask. Treatment starts as soon as the diagnosis is made.

Prevention has its own tools. Pre-exposure prophylaxis is antiretroviral medication taken by an HIV-negative person to prevent acquisition, and it is highly effective when taken as prescribed. Post exposure prophylaxis is a course started after a specific exposure — occupational needlestick, sexual exposure, or a sharps injury — and its effectiveness falls sharply the longer the interval before the first dose, so it is assessed without delay rather than at the next convenient appointment. Both are prescribed and monitored by a specialist, with baseline testing and follow-up.

Osteomyelitis: bone, joint and prosthetic infection

Infection in bone and in implanted orthopaedic hardware is one of the largest parts of this unit’s workload, and it is the clearest example of infection that cannot be cured by antibiotics alone.

Osteomyelitis reaches bone by three routes: through the bloodstream, by spread from adjacent infected tissue, or directly through trauma or surgery. Vertebral osteomyelitis — spinal infection — deserves specific mention because it presents as back pain over weeks with a raised inflammatory marker and is repeatedly treated as mechanical pain before an MRI is done. Blood cultures and, where they are negative, a biopsy for culture are what make the diagnosis, and treatment measured in weeks rather than days follows.

Prosthetic joint infection

Prosthetic joint infection is the reason bacteria on implanted metal behave differently from bacteria anywhere else. They form a biofilm — a structured community encased in a matrix they secrete — in which they divide slowly and tolerate antibiotic concentrations hundreds of times higher than the same organisms would in the bloodstream. Susceptibility testing performed on free-floating bacteria therefore predicts what will happen in a test tube, not what will happen on the implant.

The practical consequences are two. First, the diagnosis needs proper samples: multiple tissue specimens taken in theatre, not a swab of the wound surface, which grows skin organisms and misleads. Second, cure almost always requires surgery in some form — washout with retention of the implant where the infection is acute and the prosthesis is stable, or exchange of the implant in one or two stages where it is not — combined with prolonged antibiotics chosen for their activity against biofilm. This work is done jointly with orthopedics, and the plan is agreed by both specialties before the first operation rather than after the second.

Diabetic foot infection

Infection in the diabetic foot sits at the intersection of neuropathy, poor arterial supply and skin breakdown, and antibiotics address only one of the three. Assessment therefore includes the circulation, because an infected foot that is not receiving blood will not heal whatever is prescribed, and the bone, because osteomyelitis underlies a large share of deep ulcers. Care is shared with endocrinology, vascular surgery and orthopedics, and the goal stated plainly at the outset is preserving a functional foot rather than sterilising a wound.

Infective endocarditis

Infective endocarditis is infection of a heart valve or of the endocardial surface, and it is among the most demanding diagnoses in medicine because its presentation is so often mundane — weeks of low-grade fever, malaise and weight loss in someone who looks tired rather than septic. It is diagnosed by combining persistently positive blood cultures with echocardiography, and by keeping it in mind in anyone with a prosthetic valve, a pacemaker, a previous episode, or intravenous drug use.

Several features make it distinct. Multiple sets of blood cultures are taken before antibiotics because the bacteraemia is continuous and the organism determines everything that follows. A normal transthoracic echocardiogram does not exclude it, and a transoesophageal (transesophageal) study is needed where suspicion is real. Treatment is intravenous, prolonged, and measured in weeks.

Infective endocarditis treatment is a joint decision from the outset rather than a medical course with a surgical opinion attached late. Surgery is required in a substantial minority — for heart failure from valve destruction, for uncontrolled infection despite appropriate antibiotics, for abscess formation, and to prevent embolism from large mobile vegetations — and the point at which it becomes necessary is frequently earlier than instinct suggests. The team is this unit, cardiology and cardiovascular surgery reviewing the same patient together.

Line, device and surgical site infection

Anything implanted can be infected, and infection on a device follows the biofilm rules rather than the bloodstream ones.

A central line infection is diagnosed when the same organism grows from the line and from a peripheral vein, with the line cultures turning positive substantially earlier. Some organisms — Staphylococcus aureus, Candida, Pseudomonas — mean the line comes out, without an attempt at salvage. Prevention outperforms treatment here by a wide margin, and the measures are unglamorous and effective: sterile insertion, chlorhexidine skin preparation, keeping the dressing intact, and removing the line the day it stops being needed.

Surgical site infection is classified by depth, and the depth determines the response: superficial infection usually needs the wound opened and no antibiotics at all, while deep and organ-space infection needs drainage and treatment. Cardiac device infection — pacemakers and defibrillators — almost always requires complete extraction of the system, generator and leads together, because leaving hardware behind reliably reproduces the infection.

Helicobacter pylori and H pylori treatment

Helicobacter pylori colonises the stomach lining of a large share of the world’s population and is the principal cause of peptic ulcer disease and a recognised risk factor for gastric cancer. It is acquired in childhood, usually persists for life untreated, and is markedly more prevalent in this region than in northern or western Europe.

H pylori treatment is a combination of antibiotics with acid suppression taken together for a defined period, and it fails more often than patients expect — increasing clarithromycin resistance is the main reason, which is why the recommended combinations have changed over the past decade and why the regimen appropriate here is not necessarily the one someone was given elsewhere. Two principles hold regardless of which combination is used: eradication is confirmed after treatment by a breath or stool antigen test performed after an interval off acid suppression, and a course that has already failed is not simply repeated with the same drugs. Testing and treatment are managed with gastroenterology, which also owns the endoscopic assessment.

Sexually transmitted infections

The clinical content of this area is straightforward; the barrier is almost entirely that people delay seeking care. Chlamydia and gonorrhoea are frequently asymptomatic, particularly in women, and are diagnosed by nucleic acid testing on a urine sample or a self-taken swab rather than by examination. Both are curable, and gonorrhoea has become progressively more resistant, so treatment follows current susceptibility data rather than what worked a decade ago and eradication is confirmed where resistance is a concern.

Syphilis is increasing in many countries and is worth stating plainly on any page like this one, because it is easily treated when found and produces serious neurological and cardiovascular disease when it is not. Its early stages are painless and self-resolving, which is precisely why it is missed. Diagnosis is serological, treatment is well established, and partners are tested and treated.

Two habits belong with all of it. Anyone diagnosed with one sexually transmitted infection is tested for the others, including HIV, hepatitis B and syphilis, because they share routes of transmission. And partner notification is part of treatment rather than an optional courtesy, since treating one person and not the other reproduces the infection.

Travel medicine and vaccination

Travel medicine has two halves, and the second is the one this unit sees more of.

Before travel: travel vaccines, typhoid vaccine and yellow fever vaccine

Pre-travel advice is built from the itinerary rather than the country — rural and urban risk differ enormously within the same border — and from the traveller’s own health, since pregnancy, immunosuppression and chronic disease change both the risks and which vaccines can be given at all. Travel vaccines are timed to be effective: some need weeks and multiple doses, which is the main reason a consultation a few days before departure achieves less than it could.

The common ones are hepatitis A and B, typhoid vaccine for parts of South Asia, Africa and Latin America, yellow fever vaccine for parts of Africa and South America — the only one that is a legal entry requirement for some countries, given at designated centres with an official certificate — the rabies vaccine for travellers going far from medical care or working with animals, and meningococcal vaccination, which is compulsory for pilgrims travelling to Saudi Arabia. Routine adult immunity is checked at the same visit, because tetanus, measles and polio protection lapses quietly.

Malaria prophylaxis is chosen by destination, resistance pattern, duration and the traveller’s other medicines, and no regimen is completely protective, which is why mosquito-bite avoidance is part of the advice rather than an afterthought. Antimalarials are prescribed individually; the specific drug, dose and schedule belong with the doctor writing the prescription.

After travel

Fever after travel is approached with the incubation periods in mind, because they exclude as much as they suggest. Malaria is the first consideration in anyone returning from an endemic area with fever, whatever else is going on, because falciparum malaria kills quickly and is entirely treatable early; it is excluded by blood film and rapid antigen testing, repeated if the first is negative and suspicion persists. Dengue, typhoid, rickettsial infection, viral hepatitis and amoebic liver abscess make up much of the remainder. A traveller who took prophylaxis correctly can still have malaria, and travellers who grew up in an endemic country and return to visit family are at higher risk than tourists, not lower — they often take no prophylaxis and have lost the partial immunity they once had.

Diarrhoea after travel that persists beyond a couple of weeks is investigated for parasites rather than treated blindly, and antibiotics carried for self-treatment abroad are a significant source of the resistant gut organisms discussed above.

The infections of this region

This is the section that differs most from an equivalent page written in northern Europe or North America. Four infections that most Western physicians will see rarely or never are part of ordinary practice here, and a unit that sees them regularly recognises them earlier.

Brucellosis

Brucellosis is acquired from unpasteurised milk and fresh cheese made from it, and by direct contact with infected livestock. It is endemic across Anatolia, the Middle East, the Mediterranean basin and Central Asia. It causes prolonged undulating fever, drenching sweats, profound fatigue, joint and low back pain, and it is one of the classic causes of fever of unknown origin in this region. Sacroiliitis and spondylitis are characteristic, and it can also produce endocarditis, which is its main cause of death.

Two practical points define it. The laboratory must be told brucellosis is suspected, because the organism is slow-growing and hazardous to laboratory staff who are not expecting it. And treatment is a combination of antibiotics taken for weeks — never a single drug, and never a short course — because relapse after inadequate treatment is common. The dietary question patients ask most often has a simple answer: pasteurised dairy is safe, and it is fresh cheese from unpasteurised milk that carries the risk.

Hydatid disease

Hydatid disease — cystic echinococcosis — is caused by the larval stage of a tapeworm carried by dogs, with sheep as the intermediate host, and it is endemic in the sheep-raising regions of Turkey, the Middle East, North Africa, South America and Central Asia. A hydatid cyst grows slowly and silently for years, most often in the liver and next most often in the lung, and is frequently found by accident on a scan performed for something else.

The most important fact about it for anyone treating a patient here is what not to do: an undiagnosed cyst punctured or biopsied as though it were a simple fluid collection can spill its contents, seeding the abdomen and provoking a severe allergic reaction. A rounded, well-defined liver cyst in a patient from an endemic region is treated as hydatid until serology and imaging say otherwise. Management is decided by cyst stage and site, and ranges from observation of inactive calcified cysts through drug treatment and image-guided puncture-aspiration techniques to surgery, with antiparasitic cover given around any procedure. Care is shared with general surgery, radiology and, for lung cysts, thoracic surgery.

Crimean-Congo haemorrhagic fever

Crimean congo hemorrhagic fever is a tick-borne viral infection that is endemic in parts of Anatolia, the Balkans, the Caucasus, the Middle East and Africa, with cases concentrated in spring and summer among people exposed to livestock and tick habitats. It begins abruptly with fever, severe headache, muscle pain and vomiting, and in a proportion of cases progresses to bleeding and organ failure.

It matters here for two reasons beyond the illness itself. It is transmissible from person to person through blood and body fluids, which makes it one of the few infections where protecting family members and healthcare staff is part of the immediate response. And its early presentation is indistinguishable from a dozen ordinary viral illnesses, so the exposure history — rural residence, livestock contact, a recent tick bite, the time of year — is what raises it. Treatment is supportive and given in hospital with appropriate isolation; ticks are removed promptly and intact rather than burned or covered in petroleum jelly.

Leishmaniasis

Cutaneous leishmaniasis is transmitted by sandflies and is endemic in south-eastern Turkey, Syria, Iraq, Iran and much of the Middle East and North Africa. It produces a slowly enlarging skin ulcer with a raised border, painless, that persists for months and is repeatedly treated as a bacterial infection or a non-healing wound before anyone considers a parasite. Diagnosis is made from the lesion itself, and treatment depends on the species, the site and the number of lesions, ranging from local therapy to systemic treatment where lesions are extensive or cosmetically critical. Visceral leishmaniasis, which involves the spleen, liver and bone marrow, is far less common but serious and is treated systemically.

Bacterial meningitis and encephalitis

Bacterial meningitis is one of the few infections where the interval between arrival and the first dose of antibiotic measurably changes the outcome, and it is treated as an emergency in hospital everywhere. It presents with fever, headache, neck stiffness and altered consciousness, though the full combination is present in a minority — in the very young, the elderly and the immunosuppressed the picture is often confusion or drowsiness alone.

The diagnostic test is lumbar puncture, and the sequencing question that comes up constantly is whether to image the brain first. Imaging is needed where there are specific features suggesting raised intracranial pressure or a mass, and in those patients antibiotics are given before the scan rather than after it — treatment is never delayed for a test. Cerebrospinal fluid is examined for cell count, protein, glucose, Gram stain, culture and molecular testing.

Viral meningitis is far commoner and far less dangerous, usually enteroviral, and generally recovers without specific treatment. Encephalitis is a different problem: inflammation of the brain itself rather than its coverings, presenting with confusion, personality change or seizures. Herpes simplex encephalitis is the one that must not be missed because it is treatable and because untreated it causes severe permanent damage; treatment is started on suspicion and stopped if testing excludes it, rather than withheld until the result arrives. Tuberculous meningitis develops over weeks rather than hours and is the presentation of tuberculosis most often diagnosed late.

Vaccination in adults

Adult immunisation is the most cost-effective work this unit does and the most neglected. Several groups have specific needs beyond routine schedules.

• Before immunosuppression or transplantation — live vaccines cannot be given once immunosuppression has started, so the window is beforehand. Pneumococcal, influenza, hepatitis B, varicella and measles status are reviewed before biologic therapy, chemotherapy or a transplant, not after.
• After splenectomy or with a non-functioning spleen — pneumococcal, meningococcal and Haemophilus influenzae type b vaccination is essential, because overwhelming infection with encapsulated bacteria can progress within hours. This group also carries standby antibiotic advice arranged with their own physician.
• Chronic disease — diabetes, chronic kidney, liver, heart and lung disease all raise the risk from influenza and pneumococcal infection.
• Household contacts — vaccinating the family protects the person who cannot be vaccinated, which is the entire logic of protecting the immunocompromised at home.

Which vaccines apply to you, in what order and at what interval, is decided at a consultation with your records in front of the clinician. None of this is a schedule.

Treatment at home instead of in hospital

A long course of intravenous antibiotics does not require a long stay in hospital. Outpatient parenteral antibiotic therapy delivers the same treatment through a long line at home or in a day unit, and for suitable patients it removes weeks of admission along with the hospital-acquired infections, deconditioning and cost that come with it.

It requires four things in place: an infection whose treatment is genuinely established, a patient well enough and organised enough for it, a drug whose dosing schedule makes it practical, and — the part most often underestimated — a monitoring plan with named responsibility for the blood tests, the line and what happens if the fever returns. Oral switch is considered at every review rather than only at the end, since for several of the infections in this unit modern evidence supports moving to tablets earlier than tradition allows.

What this unit will not do

• Treat a culture result instead of a patient. A positive swab from a chronic wound, a colonised urinary catheter or a sputum sample from someone breathing comfortably usually reflects colonisation. Treating it produces resistance and no benefit.
• Give antibiotics for a viral illness. Most sore throats, sinus congestion and coughs are viral, and antibiotics do not shorten them. Saying so is the job even when it disappoints.
• Extend a course to be safe. Longer is not safer. Duration is set by the infection and reviewed against evidence, not against anxiety.
• Treat deep infection on hardware with drugs alone. Infected prosthetic joints, infected cardiac devices and infected lines need a surgical decision. Prescribing indefinitely around an implant that needs removing postpones the cure and generates resistance.
• Promise cure where cure does not exist. Hepatitis C is curable and we say so. Hepatitis B and HIV are controlled, not cured, and we say that too rather than allowing a hopeful misreading to stand.
• Provide antibiotics on request without an assessment. That includes courses to carry abroad, which are prescribed with an indication and instructions or not at all.

Your multidisciplinary team

The infectious disease specialist makes the diagnosis, chooses and stops the treatment, and carries the responsibility for stewardship across the hospital. The clinical microbiologist — in this country frequently the same doctor, trained in both — identifies the organism, performs susceptibility testing and calls the ward when a blood culture flags positive, which is often the moment a case changes direction. The infection prevention nurse handles isolation, contact tracing and the line and device practice that stops the next infection. The antimicrobial pharmacist checks doses against kidney and liver function, manages interactions in patients on several drugs, and runs the therapeutic drug monitoring that the older agents require.

Around them: pathology and the microbiology laboratory, hematology and medical oncology for neutropenic and immunocompromised patients, organ transplantation for the post-transplant timetable, cardiology and cardiovascular surgery for endocarditis, orthopedics for bone and prosthetic infection, gastroenterology for viral hepatitis and Helicobacter, pulmonology for tuberculosis and pneumonia, radiology for the imaging that finds the hidden focus and for image-guided drainage, and anesthesiology and intensive care for sepsis.

The international patient journey

Infectious diseases travels differently from surgery, because the commonest request is a second opinion on a treatment already underway rather than a procedure to be booked.

The first pattern is a remote review of a case that is not resolving: an infection treated with several courses without cure, a fever nobody has explained, or a culture result whose meaning is disputed. What makes this work is the microbiology in full — every culture with the organism, the site, the date and the complete susceptibility panel — together with the antibiotic history in the same detail: which drug, what dose, by which route, for how long, and why it was stopped. That last item is the most valuable and the most often missing, and without it a reviewer can only repeat what has already failed.

The second is assessment and treatment on site for a diagnosis that needs facilities: resistant infection requiring drugs that are not available everywhere, prosthetic joint or device infection needing a combined medical and surgical plan, endocarditis, or complicated tuberculosis. These are planned rather than sudden, because the surgical slot and the antibiotic course have to be scheduled together.

The third is chronic viral infection care — hepatitis B, hepatitis C and HIV — where the practical question is continuity rather than expertise. Treatment continues after departure, so the plan states which drug, which monitoring test at which interval, and who at home is responsible for each. A hepatitis C course started here and abandoned on return is worse than one never started.

Two practical notes. Bring the actual laboratory reports rather than a summary letter, and bring imaging as files rather than as printed pictures. And if you are currently on antibiotics, say so before any samples are taken — cultures drawn through treatment are the single commonest reason a diagnosis cannot be made, and a short planned pause under supervision is sometimes worth more than another test.