Infectious diseases

5 Infectious diseases


Infectious diseases remain the greatest killers of humankind. Infection differs from other disease processes in that it comprises an interaction between the human body and another organism. Infection has been part of our evolution, evident by the development of a complex immune system. All body systems are susceptible to infection, and understanding infection and its management is integral to clinical care in every medical subspecialty.



PRINCIPLES OF INFECTIOUS DISEASE


The interaction of viruses, bacteria, fungi and protozoa with the human body is:


• Symbiotic (mutually advantageous coexistence). This relationship is the most common, e.g. the numerous colonising bacteria in the human gut. Often the body benefits from this colonisation, as in the prevention of infection with Clostridium difficile by normal gut flora.

• Saprophytic (organisms colonise dead material without causing disease). Fungal skin infections are saprophytic, with minimal local damage and systemic upset.

• Parasitic (organisms are detrimental to the host). True infection occurs when organisms breach physiological barriers and enter normally sterile environments such as blood, bones, joints, internal organs or the central nervous system.


CLINICAL EXAMINATION OF THE PYREXIAL PATIENT



image


RESERVOIRS OF INFECTION



HUMAN RESERVOIRS


Infection may originate from the skin, nasopharynx or bowel, or from outside sources, often another person who may be infected or carrying a pathogen. Carriers are usually healthy and may harbour the organism in the throat (e.g. meningococci), bowel (e.g. Salmonella) or blood (e.g. hepatitis B).



ANIMAL RESERVOIRS


Animals are a significant source of human infections (zoonoses). Examples are:


• Contaminated meat/poultry (Salmonella).

• Milk (TB, brucellosis).

• Body fluids, e.g. saliva (rabies), urine (leptospirosis, Lassa fever).

• Bird faeces/secretions (psittacosis).


ENVIRONMENTAL RESERVOIRS


Environmental infective pathogens include Legionella in air conditioning or domestic water pipes, and enteropathogens (typhoid, cholera, Cryptosporidia or hepatitis A) in water supplies. The soil may harbour spores of Clostridia (tetanus) or anthrax.



TRANSMISSION OF INFECTION


This occurs by several routes:


Endogenous infection: May result from local spread, e.g. from bowel to peritoneum, or via the blood stream.


Exogenous infection: May be acquired by direct contact, aerosol inhalation, needlestick injury or a bite from an animal vector.



HEALTH CARE-ACQUIRED INFECTION (HAI)


Although community-acquired infection predominates, the transmission of infection during health care has become extremely important. HAIs affect approximately 10% of all hospital admissions and create a significant clinical and economic burden. The close proximity of compromised patients in hospitals, coupled with the concentrated use of antibiotics and the ease of transmission by health-care workers, has led to the selection of multidrug-resistant organisms such as MRSA and vancomycin-resistant enterococci (VRE). In addition, the easy spread of these organisms, plus infections such as Clostridium difficile and norovirus, may lead to outbreaks of infection necessitating ward or hospital closure.



MANAGEMENT OF INFECTION


Infectious disease results from the interaction between the microorganism and the immune system. The management of infection therefore requires both action to inhibit the microorganism and limitation of the host’s inflammatory response. This may involve more than simple antimicrobial therapy; indeed, antibiotics are not required for all infections.



PREVENTION OF INFECTION



• Reduction in the reservoirs of infection will reduce the incidence of disease produced by these organisms. Endogenous reservoirs may be reduced by chemoprophylaxis or by isolation of infective cases.

• Separation of animal sources from human hosts and rapid treatment will reduce zoonoses. Blockage of transmission by isolation and vector control will also halt the spread of infection.

• Public health measures control spread of infection and vaccination may improve ‘herd immunity’ in communities.

• Prophylactic treatment may help some individuals at high risk of infection.


VACCINATION


The potential to prevent disease by inducing immunity through vaccination remains important. There is a need both to generate new vaccines (e.g. for HIV and malaria), and to improve the efficacy of current vaccines, e.g. influenza.


The world-wide eradication of smallpox (declared by the WHO in 1980) is the best example of how successful vaccination can be in controlling infection. Vaccination becomes successful once the ‘herd immunity’ of the population reaches the required level to prevent continued spread of the wild-type virus. For example, measles requires >90% vaccination in susceptible persons before this can be achieved. Significant reductions in notifications of both measles and mumps have followed the introduction of effective vaccination schedules. From the mid-1990s in the UK, public concern about possible links of measles, mumps and rubella (MMR) vaccine to autism and inflammatory bowel disease (IBD) reduced vaccine uptake to levels that allowed reappearance of wild virus activity. The UK Medical Research Council expert group and the Commission on Human Medicines both concluded that there is no scientific evidence to link MMR to autism or IBD.



INFECTION CONTROL


HAIs have to be managed by comprehensive antibiotic policies and careful adherence to strict infection control protocols. Although environmental cleanliness and clean clothing are cosmetically important, recent evidence has confirmed the absolute importance of hand hygiene in the control of HAI. The use of alcohol hand lotion by all health-care workers between every patient contact is an effective alternative to soap and water in prevention of most HAI, but not Clostridium difficile.



OUTBREAK CONTROL


An outbreak of infection is defined as two or more linked cases of an infectious disease occurring simultaneously or unexpectedly, or the occurrence of any disease clearly in excess of normal expectancy. Many countries have systems of compulsory notification of contagious conditions to public health authorities so that outbreaks can be recognised and appropriate measures put in place to control the further spread of the condition. These measures may include:


• Source isolation.

• Quarantine of sufferers or those incubating the condition.

• Mass treatment or vaccination.


PRESENTING PROBLEMS IN INFECTIOUS DISEASES



PYREXIA OF UNKNOWN ORIGIN (PUO)


PUO is a common presenting problem and may be defined as a consistently elevated body temperature of >37.5°C persisting for >2 wks with no diagnosis after initial investigation. Many causes of PUO are listed in Box 5.1. Two or more causes of fever may coexist.



5.1 AETIOLOGY OF PUO IN DEVELOPED COUNTRIES image



Infections (30%)



• Sepsis: abscess at any site, cholecystitis/cholangitis, urinary tract infection, prostatitis, dental, sinus, bone and joint infections

• Imported infections, e.g. malaria, dengue, brucellosis

• Occult Bacterial infections; enteric fever, infective endocarditis, TB (particularly extrapulmonary)

• Enteric fevers; infective endocarditis; TB (particularly extrapulmonary)

• Viral infections (cytomegalovirus (CMV), Epstein–Barr virus (EBV), HIV); toxoplasmosis; fungal infections


Malignancy (20%)



• Lymphoma, myeloma and leukaemia; solid tumours (renal, liver, colon, stomach, pancreas)


Connective tissue disorders (15%)



• Vasculitic disorders; temporal arteritis/polymyalgia rheumatica

• Systemic lupus erythematosus (SLE); Still’s disease; polymyositis

• Rheumatic fever


Miscellaneous (20%)



• Inflammatory bowel disease; liver disease: cirrhosis, granulomatous hepatitis

• Sarcoidosis; drug reactions; atrial myxoma; thyrotoxicosis; hypothalamic lesions

• Familial Mediterranean fever


No diagnosis or resolves spontaneously (15%)



The following account applies to immunocompetent individuals in developed countries with community-acquired PUO. Infection will account for a higher percentage of PUO in developing countries. Fever in old age merits special attention (Box 5.2).



5.2 FEVER IN OLD AGE image



• Temperature measurement: fever may be missed because oral temperatures are unreliable in older people. Rectal measurement may be needed but core temperature is increasingly measured using eardrum reflectance.

• Associated acute confusion: frequent with fever, especially in those with underlying cerebrovascular disease or other causes of dementia.

• Prominent causes of PUO: include endocarditis, TB and intra-abdominal sepsis. Non-infective causes include polymyalgia rheumatica and temporal arteritis.

• Common infective causes in the very frail (e.g. nursing home residents): include pneumonia, urinary infection, soft tissue infection and gastroenteritis.

Ask about:


Travel abroad and countries of origin: Malaria, respiratory infections, viral hepatitis, typhoid and dengue are the most common causes of imported fever in the UK.

Personal and social history: Exposure to sexually transmitted infection, illicit drug use.

Occupational or recreational history: Animal exposure, consumption of unpasteurised milk.



Investigations and management



• Measure temperature and vital signs 4-hourly.

• Regularly review and expand history-taking.

• Repeat physical examination regularly for emerging signs such as cardiac murmurs, lymphadenopathy and rashes.

• Investigations should be ordered in a stepwise fashion, in order of increasing complexity and invasiveness (Boxes 5.3 and 5.4).


5.3 EARLY TESTS IN THE INVESTIGATION OF PUO IN DEVELOPED COUNTRIES image



• FBC and differential white cell count

• ESR and CRP

• Urea, creatinine and electrolytes

• LFTs, including γ-glutamyl transferase

• Blood glucose; serum ferritin; bone biochemistry; creatine phosphokinase

• Malaria blood films (if travel history)

• Urinalysis; MSU for microscopy and culture

• Faeces culture

• Sputum microscopy and culture for common pathogens and for mycobacteria

• Blood cultures × 3

• CXR; USS of abdomen

• ECG


5.4 USEFUL SEROLOGICAL INVESTIGATIONS IN THE MANAGEMENT OF PUO IN DEVELOPED COUNTRIES image


























Viral CMV, hepatitis A, B and C, infectious mononucleosis, erythrovirus, HIV, if travel history: Arbovirus
Bacterial Chlamydia, leptospirosis, Q fever, Lyme disease, brucellosis, Yersinia, Mycoplasma, Streptococcus, syphilis
If travel history Rickettsia, relapsing fever, melioidosis, bartonellosis
Fungal Cryptococcosis (antigen detection)
If travel history Histoplasmosis, coccidioidomycosis
Protozoal and parasitic Toxoplasmosis
If travel history Schistosomiasis, leishmaniasis, amoebiasis, trypanosomiasis


The role of biopsies in investigation


Liver biopsy: A low-yield investigation, with an estimated mortality of ∼0.01%, this may reveal TB, lymphoma or granulomatous disease including sarcoidosis. Biopsies should always be sent for culture, including for TB. Liver biopsy is unlikely to be helpful in patients with normal LFTs and normal liver parenchyma on imaging.


Bone marrow biopsy: Overall, the diagnostic yield of a bone marrow biopsy in PUO is ∼15%, the most commonly detected diseases being myelodysplasia, other haematological malignancies and TB. More rarely, brucellosis, enteric fever or visceral leishmaniasis may be detected, underlining the importance of sending samples for culture as well as microscopy.


Temporal artery biopsy: Should be considered in patients over the age of 50, even if the ESR is not significantly elevated. Since arteritis is patchy, diagnostic yield is increased if a 5 cm section of artery is biopsied.



Prognosis in PUO


The overall mortality of PUO is 30–40% (5% in patients aged <55 yrs, 40% in those aged >55 yrs), though if no cause is found on exhaustive investigation, the mortality is low. Older patients are more likely to have a malignancy.



FEVER IN THE RETURNING TRAVELLER/TROPICAL RESIDENT


Presentation of illness as fever is common both in patients returning from the tropics and in tropical residents. Both tropical and non-tropical infection may present after tropical travel. The most common final diagnoses in febrile patients returning from the tropics are:


• Malaria.

• Typhoid fever.

• Viral hepatitis.

• Dengue fever.

Ask about:


• Countries visited.

• Arrival and departure dates.

• Exposure to animals while abroad.

• Food/water consumed.

• Freshwater swimming.

• Sexual exposure.

• Drug use.

• Any local medicines/remedies taken.



Vaccinations and prophylaxis



• Ask about vaccinations and their validity; those against yellow fever and against hepatitis A and B virtually rule out these infections. Oral and injectable typhoid vaccinations are 70–90% effective.

• Enquire about malaria prophylaxis and establish precisely which tablets, if any, were being taken. Determine malarial resistance levels to the medicine in the country in question.


Examination


A careful examination is vital and must be repeated regularly (Fig. 5.1).


image

Fig. 5.1 Acute fever in/from the tropics: clinical examination.



Investigations


Initial investigations in all settings should start with thick and thin blood films for malaria parasites, FBC, urinalysis and CXR if indicated. Box 5.5 gives the diagnoses that should be considered in acute fever with no localising signs, grouped according to differential WCC.



5.5 DIFFERENTIAL WCC: ACUTE FEVER IN THE ABSENCE OF LOCALISING SIGNS image
















































WCC differential Potential diagnoses Further investigations
Neutrophil leucocytosis Bacterial sepsis Blood culture
Leptospira and Borrelia  
Leptospirosis Culture of blood and urine, serology
Tick-borne relapsing fever Blood film
Louse-borne relapsing fever Blood film
Amoebic liver abscess USS
Normal WCC and differential Typhoid fever Blood, stool and culture
Typhus Serology
Arboviral infection Serology (PCR and viral culture)
Lymphocytosis Viral fevers Serology
Infectious mononucleosis Monospot test
Rickettsial fevers Serology


FEVER ASSOCIATED WITH A RASH


Many infective processes produce skin manifestations, either as a result of infection or a toxin or as part of an immune reaction. Different patterns of rash associated with fever are summarised in Box 5.6. Although the combination of fever and rash frequently indicates infection in the mind of the patient, there are many non-infectious causes of this combination, such as the autoimmune vasculitides.



5.6 PATTERNS OF RASH ASSOCIATED WITH INFECTION image



Macular or maculo-papular



• Measles*, CMV, rubella, HIV seroconversion illness, enteroviral infection, typhoid and paratyphoid fevers, herpes virus type 6 infections, rickettsial infections, infectious mononucleosis, dengue fever, toxoplasmosis, secondary syphilis, drug rashes


Haemorrhagic



• Meningococcal infection, septicaemia with DIC, viral haemorrhagic fevers, rickettsial infections, leptospirosis


Urticarial



• Toxocariasis, strongyloidiasis, fascioliasis, schistosomiasis


Vesicular/pustular



• Chickenpox, hand, foot and mouth disease, shingles*, herpangina (mouth), herpes simplex infections*, poxviruses (monkey pox)


Nodular



• Erythema nodosum (primary TB and leprosy, streptococcal infection, Mycoplasma)


Erythematous



• Scarlet fever*, Lyme disease, toxic shock syndrome*, drug rashes, human erythrovirus 19 infection*, dengue fever


Chancres (ulcerating nodules)



• Syphilis, typhus (tick and mite), trypanosomiasis, anthrax, rat-bite fever


* Rash is illustrated later in this chapter.



FEVER IN THE INJECTION DRUG-USER


Ask about:


Duration: The risk of contracting hepatitis B/hepatitis C increases with each year of i.v. drug use.

Site: I.v. injection may cause DVT with infection; arterial injection may cause false aneurysm formation and compartment syndrome. Psoas abscess and septic arthritis also occur. Clostridium infection has been recorded with i.m. injection of heroin.

Technical details: Sharing of needles and spoons, and use of contaminated drugs or solvents increase the risk of infection.



Clinical assessment


Symptoms are as follows:


Breathlessness: May represent opportunistic infection secondary to HIV/immunosuppression (p. 137). Acute onset with or without pleuritic pain may indicate septic emboli from a distant injection site or from a right-sided (tricuspid or pulmonary valve) endocarditis.

Myalgia and muscle pains: May represent i.m. abscess formation; for example, flexion at the hip eliciting back pain is indicative of ilio-psoas abscess.

Abdominal pain: Opiate-induced constipation, capsular swelling in acute viral hepatitis, splenic infarct secondary to infective endocarditis.

Signs are as follows:
Skin: Necrotising infection, rashes.

Joints: Pain and redness suggest seeding from bacteraemia or direct injection into the joint space. Frequently there is associated osteomyelitis.

New murmurs or evidence of cardiac decompensation: May suggest either right- or left-sided endocarditis (check nails for splinter haemorrhages), or the cardiomyopathy of generalised sepsis. The JVP may show V waves in tricuspid endocarditis. Pleural rub or effusion is seen in DVT with PE, or septic emboli from endocarditis or infected DVT.

Neurological features: Stupor in drug overdose or hepatic encephalopathy, agitation with drug withdrawal, headache and drowsiness in meningitis or encephalitis, local paralysis or spasms with tetanus or botulism.

Legs: Groin injection sites may show abscess, false aneurysm, sinuses or haematoma. DVT or compartment syndrome may be seen in the legs. Hip flexor spasm with back pain suggests an ilio-psoas abscess.


Management


Management is that of the underlying condition. Appropriate sedative medicines should be provided for those suffering withdrawal symptoms after a long period of dependency.



FEVER IN THE NEUTROPENIC PATIENT


Neutropenia is defined as a neutrophil count of <1.5 × 109/l.


Patients with neutropenia, particularly <1.0 × 109/l, either from drug toxicity (including chemotherapy for cancer) or from marrow invasion or failure, are particularly prone to bacterial infections. Gram-positive organisms have now superseded Gram-negative infections as the most common pathogens in this condition, particularly where any line infection or indwelling catheter is present. Specimens such as blood cultures, swabs and urine samples should be taken and empirical antibiotic therapy started, commonly with a broad-spectrum penicillin and an aminoglycoside (e.g. piperacillin/tazobactam + gentamicin). Any potential nidus of infection such as a urinary or vascular catheter should be removed and, if necessary, replaced.



ACUTE DIARRHOEA


Acute diarrhoea is an extremely common presenting problem, and may result from both infectious and non-infectious causes (Box 5.7). Infectious diarrhoea is caused by faecal–oral transmission of bacterial toxins, viruses, bacteria or protozoal organisms. Psychological or physical stress may also precipitate diarrhoea. Occasionally, diarrhoea may be the presenting feature of another systemic illness, such as a lobar pneumonia.



5.7 CAUSES OF ACUTE DIARRHOEA image



Infectious



• Toxin-mediated: Bacillus cereus, clostridial spp., enterotoxin, staphylococcal enterotoxin, scombrotoxic

• Infective food poisoning: Rotavirus gastroenteritis, Shigella, Campylobacter, Clostridium difficile, Salmonella, norovirus, verocytotoxigenic E. coli, cholera, other E. coli (e.g. travellers’ diarrhoea)

• Protozoal: Giardiasis, isosporiasis, amoebic dysentery, microsporidiosis, Cryptosporidium

• Systemic illness: Sepsis (+ sepsis syndrome), pneumonia (especially ‘atypical disease’), meningococcal sepsis, malaria


Non-infectious



• GI: Acute diverticulitis, pelvic inflammatory disease, ulcerative colitis, Crohn’s disease, overflow from constipation, bowel malignancy

• Metabolic: Ketosis (e.g. diabetic decompensation), carcinoid syndrome, vasoactive intestinal peptide release, uraemia

• Drugs and toxins: NSAIDs, dinoflagellates, cytotoxic agents, plant toxins, antibiotics, heavy metals, ciguatera fish poisoning


FOOD POISONING AND GASTROENTERITIS


Acute gastroenteritis is a major cause of morbidity and mortality in both developing and developed countries. Causative organisms are listed in Boxes 5.7 and 5.8. The clinical features of food-borne disease depend on the organism; for example, enterotoxic organisms produce vomiting and ‘secretory’ watery diarrhoea. Organisms that invade the mucosa, such as Shigella and Salmonella, have longer incubation periods and may cause systemic upset and blood in the stool.



5.8 CAUSES OF BLOODY DIARRHOEA image



Infectious



• Campylobacter spp., Shigella dysentery, non-typhoidal salmonellae, enterohaemorrhagic or entero-invasive E. coli, Clostridium difficile, Vibrio parahaemolyticus, Entamoeba histolytica


Non-infectious



• Diverticular disease, rectal or colonic malignancy, inflammatory bowel disease, bleeding haemorrhoids, anal fissure, ischaemic colitis, intussusception


ASSESSMENT OF THE PATIENT WITH ACUTE DIARRHOEA


Box 5.9 shows markers of severity and coexisting conditions which increase the likelihood that intensive treatment (e.g. antimicrobials) will be needed.



5.9 SEVERITY MARKERS IN ACUTE GASTROENTERITIS image



Chronic conditions



• Age >65, diabetes mellitus, rheumatoid or other autoimmune disease, chronic renal disease, valvular heart disease (esp. with valve replacements), acquired or secondary immunodeficiency, any internal prostheses


Current drug therapy



• Diuretics, ACE inhibitors, corticosteroids, cytotoxics, proton pump or H2-receptor blockers


Current illness



• No. of stools/24 hrs, presence of blood p.r., abdominal pain, associated systemic toxicity

Ask about:


• Duration and frequency of diarrhoea.

• Presence of blood, abdominal pain and tenesmus.

• Suspect foods.

• Other family members affected.


Examination



• Record 4-hourly temperature and vital signs.

• Assess degree of dehydration by skin turgor and BP measurement.

• Measure urine output and ongoing stool losses.

• Carry out regular full abdominal examination.


Investigations



• Stool microscopy and culture.

• FBC and serum electrolytes.

• Blood film for malaria if patient has been in an affected area.


MANAGEMENT OF ACUTE DIARRHOEA


Isolation: All patients with acute, potentially infective diarrhoea should be appropriately isolated to minimise person-to-person spread of infection.


Fluid replacement: Replace established losses and ongoing losses, as well as normal daily requirements. This may be done with i.v. fluid or with oral rehydration solution (ORS).


Antibiotics/antimicrobial therapy: Not generally used, except in severe cases (Box 5.9). Have a high threshold for their use and discuss with the infectious diseases department.


Adjunctive antidiarrhoeal therapy: Anti-motility drugs are not generally recommended and may indeed prolong or worsen the course of an acute infective gastroenteritis.



CHRONIC DIARRHOEA


This is defined as diarrhoea persisting for >14 days. The differential diagnosis can be wide, and parasitic and bacterial causes, tropical malabsorption, inflammatory bowel disease and neoplasia should all be considered. Causes of chronic diarrhoea in the tropics include giardiasis, strongyloidiasis, HIV enteropathy, intestinal flukes and chronic intestinal schistosomiasis. The key signs and symptoms are:


• Diarrhoea with pale, bulky stools.

• Abdominal symptoms with distension and flatulence.

• Nutritional deficiencies.

• General ill health.

Specific causes should be treated as described later in this chapter.



EOSINOPHILIA


Eosinophilia is associated both with parasite infections (particularly helminths) and with allergic reactions. Eosinophils have an important role in mediating antibody-dependent damage to helminths. Anybody with an eosinophil count >0.4 × 109 should be investigated for both parasitic and non-parasitic causes of eosinophilia (Box 5.10). Eosinophilia is not a typical feature in malaria, amoebiasis, leishmaniasis, leprosy or tapeworm infections other than cysticercosis.



5.10 CAUSES OF EOSINOPHILIA image



• Metazoan parasite infections

• Skin diseases

• HIV

• Lymphomas

• Polyarteritis nodosa

• Hypereosinophilic syndrome

• Atopy and allergic drug reactions

• Pulmonary eosinophilia

• Human T-cell lymphotropic virus 1 (HTLV 1)

• Leukaemias

• Sarcoidosis

Ask about:


• Travel and activity abroad, e.g. freshwater bathing in sub-Saharan Africa.

• Any rashes or itching (schistosomiasis, strongyloidiasis).

• Haematuria (schistosomiasis).

• Subcutaneous swellings (loiasis, cutaneous larva migrans).



Clinical assessment


See Box 5.11.



5.11 CLINICAL FEATURES ASSOCIATED WITH HELMINTHIC INFECTIONS AND EOSINOPHILIA image



































Urticarial rashes Strongyloidiasis, onchocerciasis, fascioliasis, hydatid disease, trichinosis
Cutaneous larva migrans Ancylostoma braziliense
Dermatitis Onchocerciasis
Migratory subcutaneous swellings Loiasis, gnathostomiasis
Lymphangitis, orchitis Lymphatic filariasis
Myositis Trichinosis, cysticercosis
Febrile hepatosplenomegaly Schistosomiasis, toxocariasis
Pneumonitis Migratory stage of larval helminths (Löffler’s syndrome), lymphatic filariasis (tropical pulmonary eosinophilia), systemic strongyloidiasis
Enteritis and colitis Strongyloidiasis, capillariasis, trichinosis
Meningitis Angiostrongyliasis, strongyloidiasis


Investigations


Direct visualisation of adult worms, larvae or ova provides the best evidence. Box 5.12 lists the initial investigations for eosinophilia.



5.12 INITIAL INVESTIGATION OF EOSINOPHILIA image





























Investigation Pathogens sought
Stool microscopy Ova, cysts and parasites
Terminal urine Ova of Schistosoma haematobium
Duodenal aspirate Filariform larvae of Strongyloides, liver fluke ova
Day bloods Microfilariae Brugia malayi, Loa loa
Night bloods Microfilariae Wuchereria bancrofti
Skin snips Onchocerca volvulus
Serology Schistosoma, Filaria, Strongyloides, hydatid, trichinosis etc.


SKIN CONDITIONS IN THE RETURNING TRAVELLER/TROPICAL RESIDENT



CUTANEOUS LARVA MIGRANS (CLM)


CLM is the most common linear lesion seen in travellers. Intensely pruritic, linear, serpiginous lesions result from the larval migration of the dog hookworm (Ancylostoma caninum). The track migrates across the skin at a rate of 2–3 cm/day. Most patients have recently visited a beach where the affected part (foot, elbows, buttocks or breast) was exposed. The diagnosis is clinical, and treatment consists of topical application of 15% tiabendazole cream 12-hourly, or a single systemic dose of albendazole or ivermectin.

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Apr 3, 2017 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Infectious diseases

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