Clostridium difficile (C.diff) is a gram positive rod commonly found in hospitals. Some strains of C.diff produce exotoxins that can cause intestinal damage, leading to pseudomembranous colitis. This infection can range from mild diarrhea to severe illness. Antibiotic-associated diarrhea is often caused by C.diff, with 20-30% of cases being attributed to this bacteria. Antibiotics such as clindamycin, cephalosporins, fluoroquinolones, and broad-spectrum penicillins are frequently associated with C.diff infection.

Clinical features of C.diff infection include diarrhea, distinctive smell, abdominal pain, raised white blood cell count, and in severe cases, toxic megacolon. In some severe cases, diarrhea may be absent due to the infection causing paralytic ileus. Diagnosis is made by detecting Clostridium difficile toxin (CDT) in the stool. There are two types of exotoxins produced by C.diff, toxin A and toxin B, which cause mucosal damage and the formation of a pseudomembrane in the colon.

Risk factors for developing C.diff infection include age over 65, antibiotic treatment, previous C.diff infection, exposure to infected individuals, proton pump inhibitor or H2 receptor antagonist use, prolonged hospitalization or residence in a nursing home, and chronic disease or immunosuppression. Complications of C.diff infection can include toxic megacolon, colon perforation, sepsis, and even death, especially in frail elderly individuals.

Management of C.diff infection involves stopping the causative antibiotic if possible, optimizing hydration with IV fluids if necessary, and assessing the severity of the infection. Treatment options vary based on severity, ranging from no antibiotics for mild cases to vancomycin or fidaxomicin for moderate cases, and hospital protocol antibiotics (such as oral vancomycin with IV metronidazole) for severe or life-threatening cases. Severe cases may require admission under gastroenterology or GI surgeons.

HIV is currently not considered a notifiable disease. The Health Protection (Notification) Regulations require the reporting of certain diseases, but HIV is not included in this list. The diseases that are currently considered notifiable include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhea, invasive group A streptococcal disease, Legionnaires’ Disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, SARS, scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever. If you want to learn more about notifiable diseases and the organisms that cause them, you can refer to the Notifiable diseases and causative organisms: how to report resource.

When treating diabetic foot ulcers that are infected, the severity of the ulcer is used to determine the appropriate antimicrobial therapy. In the case of a mild foot infection (PEDIS 2 grade), the first-line treatment is typically flucloxacillin. Based on the information provided, there is no indication that pseudomonas or MRSA should be suspected. For mild infections, it is reasonable to prescribe flucloxacillin at a dosage of 500 mg-1g four times a day for a duration of 7 days. It is important to reassess the patient at the end of the treatment course.

Further Reading:

Diabetic foot is a complication that can occur in individuals with diabetes due to long-standing high blood sugar levels. This leads to a process called glycation or glycosylation, where glucose binds to proteins and lipids in the body. Abnormal protein glycation can cause cellular dysfunction and various complications.

One of the main problems in diabetic foot is peripheral vascular disease and peripheral neuropathy. These conditions can result in significant foot issues, as trauma to the feet may go unnoticed and untreated. Vascular disease also impairs wound healing and increases the risk of developing ulcers.

Clinical features of diabetic foot include reduced sensation, especially to vibration, non-dermatomal sensory loss, foot deformities such as pes cavus and claw toes, and weak or absent foot pulses. It is important for diabetic patients to have their feet assessed regularly, at least annually, to identify any potential problems. Additional foot assessments should also be conducted during hospital admissions.

During a diabetic foot assessment, the healthcare provider should remove shoes, socks, and any bandages or dressings to examine both feet. They should assess for neuropathy using a 10 g monofilament to test foot sensation and check for limb ischemia by examining pulses and performing ankle brachial pressure index (ABPI) measurements. Any abnormal tissue, such as ulcers, calluses, infections, inflammation, deformities, or gangrene, should be documented. The risk of Charcot arthropathy should also be assessed.

The severity of foot ulcers in diabetic patients can be documented using standardized systems such as SINBAD or the University of Texas classification. The presence and severity of diabetic foot infection can be determined based on criteria such as local swelling, induration, erythema, tenderness, pain, warmth, and purulent discharge.

Management of foot ulcers involves offloading, control of foot infection, control of ischemia, wound debridement, and appropriate wound dressings. Antibiotics may be necessary depending on the severity of the infection. Diabetic patients with foot ulcers should undergo initial investigations including blood tests, wound swabs, and imaging to assess for possible osteomyelitis.

Charcot foot is a serious complication of diabetic peripheral neuropathy that results in progressive destructive arthropathy and foot deformity. Signs of Charcot foot include redness, swelling, warm skin, pain, and deformity. The hallmark deformity is midfoot collapse, known as the rocker-bottom foot.

Public Health England (PHE) has a primary goal of promptly identifying potential disease outbreaks and epidemics. While accuracy of diagnosis is important, it is not the main focus. Since 1968, the clinical suspicion of a notifiable infection has been sufficient for reporting purposes.

Registered medical practitioners (RMPs) are legally obligated to notify the designated proper officer at their local council or local health protection team (HPT) when they suspect cases of certain infectious diseases.

The Health Protection (Notification) Regulations 2010 specify the diseases that RMPs must report to the proper officers. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, severe acute respiratory syndrome (SARS), scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.

It is worth noting that leptospirosis is not considered a notifiable disease, making it the least likely option among the diseases listed above.

Reported parental perception of a fever should be regarded as valid and taken seriously by healthcare professionals.

For infants under the age of 4 weeks, it is recommended to measure body temperature using an electronic thermometer in the axilla.

In children aged 4 weeks to 5 years, body temperature can be measured using one of the following methods: an electronic thermometer in the axilla, a chemical dot thermometer in the axilla, or an infra-red tympanic thermometer.

It is important to note that oral and rectal routes should not be utilized for temperature measurement in this age group. Additionally, forehead chemical thermometers are not reliable and should be avoided.

The estimated median incubation period from HIV infection to the onset of advanced HIV disease, also known as AIDS, is around ten years.

Based on the patient’s symptoms and medical history, the most likely organism responsible for this case of infective endocarditis is Streptococcus viridans. This is because the patient has a history of aortic stenosis, which is a risk factor for developing infective endocarditis. Additionally, the patient had a tooth extraction prior to the onset of symptoms, which can introduce bacteria into the bloodstream and increase the risk of infective endocarditis. Streptococcus viridans is a common cause of infective endocarditis, particularly in patients with underlying heart valve disease.

Further Reading:

Infective endocarditis (IE) is an infection that affects the innermost layer of the heart, known as the endocardium. It is most commonly caused by bacteria, although it can also be caused by fungi or viruses. IE can be classified as acute, subacute, or chronic depending on the duration of illness. Risk factors for IE include IV drug use, valvular heart disease, prosthetic valves, structural congenital heart disease, previous episodes of IE, hypertrophic cardiomyopathy, immune suppression, chronic inflammatory conditions, and poor dental hygiene.

The epidemiology of IE has changed in recent years, with Staphylococcus aureus now being the most common causative organism in most industrialized countries. Other common organisms include coagulase-negative staphylococci, streptococci, and enterococci. The distribution of causative organisms varies depending on whether the patient has a native valve, prosthetic valve, or is an IV drug user.

Clinical features of IE include fever, heart murmurs (most commonly aortic regurgitation), non-specific constitutional symptoms, petechiae, splinter hemorrhages, Osler’s nodes, Janeway’s lesions, Roth’s spots, arthritis, splenomegaly, meningism/meningitis, stroke symptoms, and pleuritic pain.

The diagnosis of IE is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Major criteria include positive blood cultures with typical microorganisms and positive echocardiogram findings. Minor criteria include fever, vascular phenomena, immunological phenomena, and microbiological phenomena. Blood culture and echocardiography are key tests for diagnosing IE.

In summary, infective endocarditis is an infection of the innermost layer of the heart that is most commonly caused by bacteria. It can be classified as acute, subacute, or chronic and can be caused by a variety of risk factors. Staphylococcus aureus is now the most common causative organism in most industrialized countries. Clinical features include fever, heart murmurs, and various other symptoms. The diagnosis is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Blood culture and echocardiography are important tests for diagnosing IE.

This man is at high risk of contracting HIV due to his history of intravenous drug abuse and sharing needles. If a patient has a flu-like illness and a history of risk factors, it is important to suspect that they may be experiencing an HIV seroconversion illness.

Around 20-60% of individuals who contract HIV go through a seroconversion illness. This typically occurs within 1 to 6 weeks after exposure and presents with symptoms similar to the flu. Common clinical features include fever, malaise, myalgia, pharyngitis, diarrhea, headaches, maculopapular rash, lymphadenopathy, and neuralgia.

During this stage of the disease, antibody tests will show negative results. However, a diagnosis of HIV can still be made by conducting a P24 antigen test or measuring HIV RNA levels. CD4 and CD8 counts are usually within the normal range at this stage.

This patient is showing signs and symptoms that align with a C.diff infection. They also have several risk factors that increase their likelihood of developing this infection, including being over the age of 65, residing in a nursing home or being hospitalized for an extended period, recent use of antibiotics, and regular use of PPI medication.

Further Reading:

Clostridium difficile (C.diff) is a gram positive rod commonly found in hospitals. Some strains of C.diff produce exotoxins that can cause intestinal damage, leading to pseudomembranous colitis. This infection can range from mild diarrhea to severe illness. Antibiotic-associated diarrhea is often caused by C.diff, with 20-30% of cases being attributed to this bacteria. Antibiotics such as clindamycin, cephalosporins, fluoroquinolones, and broad-spectrum penicillins are frequently associated with C.diff infection.

Clinical features of C.diff infection include diarrhea, distinctive smell, abdominal pain, raised white blood cell count, and in severe cases, toxic megacolon. In some severe cases, diarrhea may be absent due to the infection causing paralytic ileus. Diagnosis is made by detecting Clostridium difficile toxin (CDT) in the stool. There are two types of exotoxins produced by C.diff, toxin A and toxin B, which cause mucosal damage and the formation of a pseudomembrane in the colon.

Risk factors for developing C.diff infection include age over 65, antibiotic treatment, previous C.diff infection, exposure to infected individuals, proton pump inhibitor or H2 receptor antagonist use, prolonged hospitalization or residence in a nursing home, and chronic disease or immunosuppression. Complications of C.diff infection can include toxic megacolon, colon perforation, sepsis, and even death, especially in frail elderly individuals.

Management of C.diff infection involves stopping the causative antibiotic if possible, optimizing hydration with IV fluids if necessary, and assessing the severity of the infection. Treatment options vary based on severity, ranging from no antibiotics for mild cases to vancomycin or fidaxomicin for moderate cases, and hospital protocol antibiotics (such as oral vancomycin with IV metronidazole) for severe or life-threatening cases. Severe cases may require admission under gastroenterology or GI surgeons.

The Health Protection (Notification) Regulations currently require the reporting of certain diseases. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ Disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, SARS, scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.

Public Health England (PHE) has the primary goal of promptly identifying potential disease outbreaks and epidemics. While accuracy of diagnosis is not the main focus, clinical suspicion of a notifiable infection has been sufficient since 1968.

Registered medical practitioners (RMPs) are legally obligated to inform the designated proper officer at their local council or local health protection team (HPT) about suspected cases of specific infectious diseases.

The Health Protection (Notification) Regulations 2010 outline the diseases that RMPs must report to the proper officers at local authorities. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, severe acute respiratory syndrome (SARS), scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.

Two types of tapeworms, Taenia solium and Taenia saginata, can infest humans. Infestation occurs when people consume meat from intermediate hosts that contain the parasite’s tissue stages. Tapeworms compete for nutrients and infestation is often without symptoms. However, in more severe cases, individuals may experience epigastric pain, diarrhea, and vomiting. Diagnosis involves identifying characteristic eggs in the patient’s stool.

Taenia solium infestation can also lead to a condition called cysticercosis. This occurs when larval cysts infiltrate and spread throughout the lung, liver, eye, or brain. Cysticercosis presents with neurological symptoms, seizures, and impaired vision. Confirmation of cysticercosis involves the presence of antibodies and imaging tests such as chest X-rays and CT brain scans.

The treatment for tapeworm infestation is highly effective and involves the use of medications like niclosamide or praziquantel. However, it is important to seek specialist advice when managing Taenia infections in the central nervous system, as severe inflammatory reactions can occur.

For patients with sepsis and hypotension, it is recommended to administer 30ml of crystalloid fluid per kilogram of body weight. However, if the patient does not have acute kidney injury, is not hypotensive, and has a lactate level below 2 mmol/l, a 500ml immediate dose may be given.

Further Reading:

There are multiple definitions of sepsis, leading to confusion among healthcare professionals. The Sepsis 3 definition describes sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection. The Sepsis 2 definition includes infection plus two or more SIRS criteria. The NICE definition states that sepsis is a clinical syndrome triggered by the presence of infection in the blood, activating the body’s immune and coagulation systems. The Sepsis Trust defines sepsis as a dysregulated host response to infection mediated by the immune system, resulting in organ dysfunction, shock, and potentially death.

The confusion surrounding sepsis terminology is further compounded by the different versions of sepsis definitions, known as Sepsis 1, Sepsis 2, and Sepsis 3. The UK organizations RCEM and NICE have not fully adopted the changes introduced in Sepsis 3, causing additional confusion. While Sepsis 3 introduces the use of SOFA scores and abandons SIRS criteria, NICE and the Sepsis Trust have rejected the use of SOFA scores and continue to rely on SIRS criteria. This discrepancy creates challenges for emergency department doctors in both exams and daily clinical practice.

To provide some clarity, RCEM now recommends referring to national standards organizations such as NICE, SIGN, BTS, or others relevant to the area. The Sepsis Trust, in collaboration with RCEM and NICE, has published a toolkit that serves as a definitive reference point for sepsis management based on the sepsis 3 update.

There is a consensus internationally that the terms SIRS and severe sepsis are outdated and should be abandoned. Instead, the terms sepsis and septic shock should be used. NICE defines septic shock as a life-threatening condition characterized by low blood pressure despite adequate fluid replacement and organ dysfunction or failure. Sepsis 3 defines septic shock as persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more, along with a serum lactate level greater than 2 mmol/l despite adequate volume resuscitation.

NICE encourages clinicians to adopt an approach of considering sepsis in all patients, rather than relying solely on strict definitions. Early warning or flag systems can help identify patients with possible sepsis.

This individual is experiencing early symptoms such as tiredness, swollen tonsils with discharge, enlarged lymph nodes, and an enlarged liver. Additionally, they fall within the typical age group for developing glandular fever (infectious mononucleosis). Epstein-Barr virus (EBV) is responsible for the majority of glandular fever cases.

Further Reading:

Glandular fever, also known as infectious mononucleosis or mono, is a clinical syndrome characterized by symptoms such as sore throat, fever, and swollen lymph nodes. It is primarily caused by the Epstein-Barr virus (EBV), with other viruses and infections accounting for the remaining cases. Glandular fever is transmitted through infected saliva and primarily affects adolescents and young adults. The incubation period is 4-8 weeks.

The majority of EBV infections are asymptomatic, with over 95% of adults worldwide having evidence of prior infection. Clinical features of glandular fever include fever, sore throat, exudative tonsillitis, lymphadenopathy, and prodromal symptoms such as fatigue and headache. Splenomegaly (enlarged spleen) and hepatomegaly (enlarged liver) may also be present, and a non-pruritic macular rash can sometimes occur.

Glandular fever can lead to complications such as splenic rupture, which increases the risk of rupture in the spleen. Approximately 50% of splenic ruptures associated with glandular fever are spontaneous, while the other 50% follow trauma. Diagnosis of glandular fever involves various investigations, including viral serology for EBV, monospot test, and liver function tests. Additional serology tests may be conducted if EBV testing is negative.

Management of glandular fever involves supportive care and symptomatic relief with simple analgesia. Antiviral medication has not been shown to be beneficial. It is important to identify patients at risk of serious complications, such as airway obstruction, splenic rupture, and dehydration, and provide appropriate management. Patients can be advised to return to normal activities as soon as possible, avoiding heavy lifting and contact sports for the first month to reduce the risk of splenic rupture.

Rare but serious complications associated with glandular fever include hepatitis, upper airway obstruction, cardiac complications, renal complications, neurological complications, haematological complications, chronic fatigue, and an increased risk of lymphoproliferative cancers and multiple sclerosis.

Prophylactic VZIG is recommended for individuals at high risk who have had a significant exposure to varicella-zoster but have no known immunity (meaning they have not had chickenpox before). High-risk groups include neonates, pregnant women, the immunocompromised, and those on high dose steroids. For children on more than 2 mg/kg/day for more than 14 days, or adults on 40 mg/day for more than a week, it is important to temporarily increase their steroid dose during times of infection or stress. Stopping or reducing the dose of prednisolone would not be appropriate in this case. This patient is at high risk of adrenal insufficiency. Severe varicella infection can occur, leading to complications such as pneumonia, hepatitis, and DIC. It is important to note that varicella infection may not present with the typical rash and can have atypical or insidious symptoms. If a patient on high dose steroids develops varicella infection, they should be admitted for specialist review and receive intravenous aciclovir.

Glandular fever is typically treated with conservative management. It is a self-limiting illness that usually resolves within 2-4 weeks and can be effectively managed with over-the-counter pain relievers. Patients should also be informed about the expected duration of the illness, ways to minimize transmission, precautions to prevent complications like splenic rupture, and provided with appropriate support and guidance. These measures are outlined in the following notes.

Further Reading:

Glandular fever, also known as infectious mononucleosis or mono, is a clinical syndrome characterized by symptoms such as sore throat, fever, and swollen lymph nodes. It is primarily caused by the Epstein-Barr virus (EBV), with other viruses and infections accounting for the remaining cases. Glandular fever is transmitted through infected saliva and primarily affects adolescents and young adults. The incubation period is 4-8 weeks.

The majority of EBV infections are asymptomatic, with over 95% of adults worldwide having evidence of prior infection. Clinical features of glandular fever include fever, sore throat, exudative tonsillitis, lymphadenopathy, and prodromal symptoms such as fatigue and headache. Splenomegaly (enlarged spleen) and hepatomegaly (enlarged liver) may also be present, and a non-pruritic macular rash can sometimes occur.

Glandular fever can lead to complications such as splenic rupture, which increases the risk of rupture in the spleen. Approximately 50% of splenic ruptures associated with glandular fever are spontaneous, while the other 50% follow trauma. Diagnosis of glandular fever involves various investigations, including viral serology for EBV, monospot test, and liver function tests. Additional serology tests may be conducted if EBV testing is negative.

Management of glandular fever involves supportive care and symptomatic relief with simple analgesia. Antiviral medication has not been shown to be beneficial. It is important to identify patients at risk of serious complications, such as airway obstruction, splenic rupture, and dehydration, and provide appropriate management. Patients can be advised to return to normal activities as soon as possible, avoiding heavy lifting and contact sports for the first month to reduce the risk of splenic rupture.

Rare but serious complications associated with glandular fever include hepatitis, upper airway obstruction, cardiac complications, renal complications, neurological complications, haematological complications, chronic fatigue, and an increased risk of lymphoproliferative cancers and multiple sclerosis.

Typhoid fever is a bacterial infection caused by Salmonella typhi. Paratyphoid fever, on the other hand, is a similar illness caused by Salmonella paratyphi. Together, these two conditions are collectively known as the enteric fevers.

Typhoid fever is prevalent in India and many other parts of Asia, Africa, Central America, and South America. It is primarily transmitted through the consumption of contaminated food or water that has been infected by the feces of an acutely infected or recovering person, or a chronic carrier. About 1-6% of individuals infected with S. typhi become chronic carriers. The incubation period for this illness ranges from 7 to 21 days.

During the first week of the illness, patients experience weakness and lethargy, accompanied by a gradually increasing fever. The onset of the illness is usually subtle, and constipation is more common than diarrhea in the early stages. Other early symptoms include headaches, abdominal pain, and nosebleeds. In cases of typhoid fever, the fever can occur with a relatively slow heart rate, known as Faget’s sign.

As the illness progresses into the second week, patients often become too fatigued to get out of bed. Diarrhea becomes more prominent, the fever intensifies, and patients may become agitated and delirious. The abdomen may become tender and swollen, and approximately 75% of patients develop an enlarged spleen. In up to a third of patients, red macules known as Rose spots may appear.

In the third week, the illness can lead to various complications. Intestinal bleeding may occur due to bleeding in congested Peyer’s patches. Other potential complications include intestinal perforation, secondary pneumonia, encephalitis, myocarditis, metastatic abscesses, and septic shock.

After the third week, surviving patients begin to show signs of improvement, with the fever and symptoms gradually subsiding over the course of 7-14 days. Untreated patients have a mortality rate of 15-30%. Traditionally, drugs like ampicillin and trimethoprim have been used for treatment. However, due to the emergence of multidrug resistant cases, azithromycin or fluoroquinolones are now the primary treatment options.

Plasmodium falciparum malaria is transmitted by female mosquitoes of the Anopheles genus. While it can be found worldwide, it is most prevalent in Africa. The incubation period for this type of malaria is typically between 7 to 14 days.

The parasite, known as sporozoites, invades hepatocytes (liver cells). Inside the hepatocyte, the parasite undergoes asexual reproduction, resulting in the production of merozoites. These merozoites are then released into the bloodstream and invade the red blood cells of the host.

Currently, the recommended treatment for P. falciparum malaria is artemisinin-based combination therapy (ACT). This involves combining fast-acting artemisinin-based compounds with drugs from different classes. Some of the companion drugs used in ACT include lumefantrine, mefloquine, amodiaquine, sulfadoxine/pyrimethamine, piperaquine, and chlorproguanil/dapsone. Artemisinin derivatives such as dihydroartemisinin, artesunate, and artemether are also used.

In cases where artemisinin combination therapy is not available, oral quinine or atovaquone with proguanil hydrochloride can be used as alternatives. However, quinine is not well-tolerated for prolonged treatment and should be combined with another drug, typically oral doxycycline (or clindamycin for pregnant women and young children).

For severe or complicated cases of falciparum malaria, it is recommended to manage the patient in a high dependency unit or intensive care setting. Intravenous artesunate is indicated for all patients with severe or complicated falciparum malaria, as well as those at high risk of developing severe disease (e.g., if more than 2% of red blood cells are parasitized) or if the patient is unable to take oral treatment. After a minimum of 24 hours of intravenous artesunate treatment and once the patient has shown improvement and can tolerate oral treatment, a full course of artemisinin combination therapy should be administered.

Public Health England (PHE) has a primary goal of swiftly identifying potential disease outbreaks and epidemics. While accuracy of diagnosis is important, it is not the main focus. Since 1968, clinical suspicion of a notifiable infection has been sufficient for reporting.
Registered medical practitioners (RMPs) are legally obligated to notify the designated proper officer at their local council or local health protection team (HPT) if they suspect cases of certain infectious diseases.
The Health Protection (Notification) Regulations 2010 specify the diseases that RMPs must report to the proper officers at local authorities. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, severe acute respiratory syndrome (SARS), scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.
It is worth noting that roseola infantum is not considered a notifiable disease, making it the least likely option among the diseases listed above.

Norovirus is the leading cause of gastroenteritis in adults in the UK. Viruses are responsible for the majority of cases of infectious diarrhea, with norovirus being the most common culprit in adults. Among young children, rotavirus is the primary pathogen, although its prevalence has decreased since the introduction of a rotavirus vaccine. As of 2023, rotavirus remains the most common cause of viral gastroenteritis in children.

Further Reading:

Gastroenteritis is a transient disorder characterized by the sudden onset of diarrhea, with or without vomiting. It is caused by enteric infections with viruses, bacteria, or parasites. The most common viral causes of gastroenteritis in adults include norovirus, rotavirus, and adenovirus. Bacterial pathogens such as Campylobacter jejuni and coli, Escherichia coli, Clostridium perfringens, Bacillus cereus, Staphylococcus aureus, Salmonella typhi and paratyphi, and Shigella dysenteriae, flexneri, boydii, and sonnei can also cause gastroenteritis. Parasites such as Cryptosporidium, Entamoeba histolytica, and Giardia intestinalis or Giardia lamblia can also lead to diarrhea.

Diagnosis of gastroenteritis is usually based on clinical symptoms, and investigations are not required in many cases. However, stool culture may be indicated in certain situations, such as when the patient is systemically unwell or immunocompromised, has acute painful diarrhea or blood in the stool suggesting dysentery, has recently taken antibiotics or acid-suppressing medications, or has not resolved diarrhea by day 7 or has recurrent diarrhea.

Management of gastroenteritis in adults typically involves advice on oral rehydration. Intravenous rehydration and more intensive treatment may be necessary for patients who are systemically unwell, exhibit severe dehydration, or have intractable vomiting or high-output diarrhea. Antibiotics are not routinely required unless a specific organism is identified that requires treatment. Antidiarrheal drugs, antiemetics, and probiotics are not routinely recommended.

Complications of gastroenteritis can occur, particularly in young children, the elderly, pregnant women, and immunocompromised individuals. These complications include dehydration, electrolyte disturbance, acute kidney injury, haemorrhagic colitis, haemolytic uraemic syndrome, reactive arthritis, Reiter’s syndrome, aortitis, osteomyelitis, sepsis, toxic megacolon, pancreatitis, sclerosing cholangitis, liver cirrhosis, weight loss, chronic diarrhea, irritable bowel syndrome, inflammatory bowel disease, acquired lactose intolerance, Guillain-Barré syndrome, meningitis, invasive entamoeba infection, and liver abscesses.

Public Health England (PHE) has a primary goal of swiftly identifying potential disease outbreaks and epidemics. While accuracy of diagnosis is important, it takes a backseat to the speed of detection. Since 1968, the clinical suspicion of a notifiable infection has been sufficient for reporting purposes.

Registered medical practitioners (RMPs) are legally obligated to notify the designated proper officer at their local council or local health protection team (HPT) when they suspect cases of certain infectious diseases.

The Health Protection (Notification) Regulations 2010 specify the diseases that RMPs must report to the proper officers. These diseases include acute encephalitis, acute infectious hepatitis, acute meningitis, acute poliomyelitis, anthrax, botulism, brucellosis, cholera, COVID-19, diphtheria, enteric fever (typhoid or paratyphoid fever), food poisoning, haemolytic uraemic syndrome (HUS), infectious bloody diarrhoea, invasive group A streptococcal disease, Legionnaires’ disease, leprosy, malaria, measles, meningococcal septicaemia, mumps, plague, rabies, rubella, severe acute respiratory syndrome (SARS), scarlet fever, smallpox, tetanus, tuberculosis, typhus, viral haemorrhagic fever (VHF), whooping cough, and yellow fever.

It is worth noting that influenza is not considered a notifiable disease, making it the least likely option among the diseases listed above.

Respiratory alkalosis can be caused by hyperventilation, such as during periods of anxiety. It can also be a result of conditions like pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, or the early stages of aspirin overdose.

Respiratory acidosis is often associated with chronic obstructive pulmonary disease (COPD) or life-threatening asthma. Other causes include pulmonary edema, sedative drug overdose (such as opiates or benzodiazepines), neuromuscular disease, obesity, or certain medications.

Metabolic alkalosis can occur due to vomiting, potassium depletion (often caused by diuretic usage), Cushing’s syndrome, or Conn’s syndrome.

Metabolic acidosis with a raised anion gap can be caused by conditions like lactic acidosis (which can result from hypoxemia, shock, sepsis, or infarction) or ketoacidosis (commonly seen in diabetes, starvation, or alcohol excess). Other causes include renal failure or poisoning (such as late stages of aspirin overdose, methanol, or ethylene glycol).

Metabolic acidosis with a normal anion gap can be attributed to conditions like renal tubular acidosis, diarrhea, ammonium chloride ingestion, or adrenal insufficiency.

Plasmodium falciparum malaria is transmitted by female mosquitoes of the Anopheles genus. The Aedes genus, on the other hand, is responsible for spreading diseases like dengue fever and yellow fever. The parasite enters hepatocytes and undergoes asexual reproduction, resulting in the release of merozoites into the bloodstream. These merozoites then invade the red blood cells of the host. The incubation period for Plasmodium falciparum malaria ranges from 7 to 14 days.

The main symptom of malaria is known as the malarial paroxysm, which consists of a cyclical pattern of cold chills, followed by a stage of intense heat, and finally a period of profuse sweating as the fever subsides. However, some individuals may experience a continuous fever instead.

Currently, the recommended treatment for P. falciparum malaria is artemisinin-based combination therapy (ACT). This involves combining fast-acting artemisinin-based compounds with drugs from a different class. Companion drugs used in ACT include lumefantrine, mefloquine, amodiaquine, sulfadoxine/pyrimethamine, piperaquine, and chlorproguanil/dapsone. Artemisinin derivatives such as dihydroartemisinin, artesunate, and artemether are also used.

If artemisinin combination therapy is not available, oral quinine or atovaquone with proguanil hydrochloride can be used as an alternative. However, quinine is not well-tolerated for prolonged treatment and should be combined with another drug, typically oral doxycycline (or clindamycin for pregnant women and young children).

Severe or complicated cases of falciparum malaria require specialized care in a high dependency unit or intensive care setting. Intravenous artesunate is recommended for all patients with severe or complicated falciparum malaria, as well as those at high risk of developing severe disease (e.g., if more than 2% of red blood cells are parasitized) or if the patient is unable to take oral treatment. After a minimum of 24 hours of intravenous artesunate treatment and improvement in the patient’s condition, a full course of artemisinin combination therapy should be administered orally.

The tricuspid valve is the most commonly affected valve in cases of infective endocarditis among intravenous drug users. This means that when IV drug users develop infective endocarditis, it is most likely to affect the tricuspid valve. On the other hand, in cases of native valve endocarditis and prosthetic valve endocarditis, the mitral valve is the valve that is most commonly affected.

Further Reading:

Infective endocarditis (IE) is an infection that affects the innermost layer of the heart, known as the endocardium. It is most commonly caused by bacteria, although it can also be caused by fungi or viruses. IE can be classified as acute, subacute, or chronic depending on the duration of illness. Risk factors for IE include IV drug use, valvular heart disease, prosthetic valves, structural congenital heart disease, previous episodes of IE, hypertrophic cardiomyopathy, immune suppression, chronic inflammatory conditions, and poor dental hygiene.

The epidemiology of IE has changed in recent years, with Staphylococcus aureus now being the most common causative organism in most industrialized countries. Other common organisms include coagulase-negative staphylococci, streptococci, and enterococci. The distribution of causative organisms varies depending on whether the patient has a native valve, prosthetic valve, or is an IV drug user.

Clinical features of IE include fever, heart murmurs (most commonly aortic regurgitation), non-specific constitutional symptoms, petechiae, splinter hemorrhages, Osler’s nodes, Janeway’s lesions, Roth’s spots, arthritis, splenomegaly, meningism/meningitis, stroke symptoms, and pleuritic pain.

The diagnosis of IE is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Major criteria include positive blood cultures with typical microorganisms and positive echocardiogram findings. Minor criteria include fever, vascular phenomena, immunological phenomena, and microbiological phenomena. Blood culture and echocardiography are key tests for diagnosing IE.

In summary, infective endocarditis is an infection of the innermost layer of the heart that is most commonly caused by bacteria. It can be classified as acute, subacute, or chronic and can be caused by a variety of risk factors. Staphylococcus aureus is now the most common causative organism in most industrialized countries. Clinical features include fever, heart murmurs, and various other symptoms. The diagnosis is based on the modified Duke criteria, which require the presence of certain major and minor criteria. Blood culture and echocardiography are important tests for diagnosing IE.

This explanation suggests that the patient’s symptoms are consistent with a case of travellers diarrhoea, which is in line with their medical history. GBS typically occurs within 1-3 weeks after the initial viral or bacterial infection that caused it.

Further Reading:

Campylobacter jejuni is a common cause of gastrointestinal infections, particularly travellers diarrhoea. It is a gram-negative bacterium that appears as curved rods. The infection is transmitted through the feco-oral route, often through the ingestion of contaminated meat, especially poultry. The incubation period for Campylobacter jejuni is typically 1-7 days, and the illness usually lasts for about a week.

The main symptoms of Campylobacter jejuni infection include watery, and sometimes bloody, diarrhea accompanied by abdominal cramps, fever, malaise, and headache. In some cases, complications can arise from the infection. Guillain-Barre syndrome (GBS) is one such complication that is associated with Campylobacter jejuni. Approximately 30% of GBS cases are caused by this bacterium.

When managing Campylobacter jejuni infection, conservative measures are usually sufficient, with a focus on maintaining hydration. However, in cases where symptoms are severe, such as high fever, bloody diarrhea, or high-output diarrhea, or if the person is immunocompromised, antibiotics may be necessary. NICE recommends the use of clarithromycin, administered at a dose of 250-500 mg twice daily for 5-7 days, starting within 3 days of the onset of illness.

A normal CD4 count ranges from 500-1000 cells/mm3. In individuals diagnosed with HIV, the CD4 count is typically monitored every 3-6 months. It is important to note that the CD4 count can fluctuate on a daily basis and can be influenced by the timing of the blood test as well as the presence of other infections or illnesses.

When the CD4 count falls below 350 cells/mm3, it is recommended to consider starting antiretroviral therapy. A CD4 count below 200 cells/mm3 is indicative of advanced HIV disease, also known as AIDS defining.

The risk of acquiring HIV from an HIV positive source patient ranges from 0.2% to 0.5%. On the other hand, the risk of contracting Hepatitis C from a Hepatitis C positive source patient is estimated to be between 3% and 10%.

When it comes to post-exposure prophylaxis for HIV, it is crucial to administer it within 72 hours after a needle-stick injury. The effectiveness of this prophylaxis decreases with time, so it should be given as soon as possible after the incident. For detailed guidelines on post-exposure prophylaxis, please refer to the DOH guidelines.

Unfortunately, there is currently no post-exposure prophylaxis available for Hepatitis C. However, there is a class of antiviral medications called nucleotide polymerase inhibitors that have revolutionized the treatment of Hepatitis C. These medications, such as sofosbuvir and daclatasvir, have shown remarkable efficacy in curing more than 90% of people with Hepatitis C. Moreover, they are easier to tolerate and have shorter treatment courses, making them a significant advancement in Hepatitis C treatment.

This patient has returned from West Africa exhibiting symptoms and signs consistent with a viral haemorrhagic fever, which strongly suggests a diagnosis of Ebola. Ebola, also known as Ebola haemorrhagic fever, is caused by RNA viruses belonging to the Ebola Virus genus. The virus is zoonotic, meaning it can be transmitted from animals to humans, with fruit bats believed to be the natural reservoir. It spreads through direct contact with bodily fluids and may also be transmitted through sexual intercourse. The incubation period typically ranges from 4 to 10 days, but it can extend up to 3 weeks.

The initial manifestations of the disease usually resemble those of a flu-like illness, characterized by fever, muscle pain, and headaches. However, the condition rapidly deteriorates, leading to worsening fever, vomiting, diarrhea, and abdominal pain. In a significant proportion of cases (30-50%), patients develop internal and external bleeding, presenting with petechiae, purpura, epistaxis, gastrointestinal bleeding, and bleeding from the urinary tract. Therefore, immediate isolation of suspected Ebola cases is crucial, followed by prompt transportation to a High-Level Isolation Unit. Contacting the Health Protection Team and initiating comprehensive public health measures is essential.

Healthcare staff involved in the management of suspected Ebola cases must adhere to strict personal protection protocols. This includes practicing thorough hand hygiene, wearing double gloves, utilizing fluid repellent disposable coveralls or gowns, donning full-length plastic aprons over the coveralls or gowns, wearing head covers such as surgical caps, using fluid repellent footwear like surgical boots, and wearing full face shields or goggles along with fluid repellent FFP3 respirators.

The management of Ebola primarily focuses on providing supportive care, often requiring intensive care treatment if available. The mortality rate of Ebola varies across different outbreaks, ranging from 50% to 90%. Death frequently occurs as a result of hypovolemic shock.

Malaria is a contagious illness that is spread by female mosquitoes of the Anopheles genus. It is caused by a parasitic infection from the Plasmodium genus. There are five species of Plasmodium that can cause disease in humans: Plasmodium falciparum, Plasmodium ovale, Plasmodium vivax, Plasmodium malariae, and Plasmodium knowlesi.

The main symptom of malaria is the malarial paroxysm, which is a recurring cycle of cold, hot, and sweating stages. During the cold stage, the patient experiences intense chills, followed by an extremely hot stage, and finally a stage of profuse sweating. Upon examination, the patient may show signs of anemia, jaundice, and have an enlarged liver and spleen, but no signs of swollen lymph nodes.

Plasmodium falciparum is the most severe form of malaria and is responsible for the majority of deaths. Severe or complicated malaria is indicated by impaired consciousness, seizures, low blood sugar, anemia, kidney damage, difficulty breathing, and spontaneous bleeding. Given the presentation, it is likely that this case involves Plasmodium falciparum.

Currently, artemisinin-based combination therapy (ACT) is recommended for treating P. falciparum malaria. This involves combining fast-acting artemisinin-based compounds with a drug from a different class. Companion drugs include lumefantrine, mefloquine, amodiaquine, sulfadoxine/pyrimethamine, piperaquine, and chlorproguanil/dapsone. Artemisinin derivatives include dihydroartemisinin, artesunate, and artemether.

If ACT is not available, oral quinine or atovaquone with proguanil hydrochloride can be used. Quinine is highly effective but not well tolerated for long-term treatment, so it should be combined with another drug, usually oral doxycycline (or clindamycin for pregnant women and young children).

Severe or complicated falciparum malaria should be managed in a high dependency unit or intensive care setting. Intravenous artesunate is recommended for all patients with severe or complicated falciparum malaria, or those at high risk of developing severe disease (such as if more than 2% of red blood cells are infected), or

The traffic light system is a useful tool for evaluating the potential risk of serious illness in children. This system categorizes clinical features into three groups based on severity: red (high-risk), amber (intermediate-risk), and green (low-risk).

Children displaying any of the following symptoms or signs fall into the high-risk group for serious illness: pale/mottled/ashen/blue skin, lips or tongue; lack of response to social cues; appearing unwell to a healthcare professional; inability to wake or stay awake when roused; weak, high-pitched, or continuous cry; grunting; respiratory rate exceeding 60 breaths per minute; moderate or severe chest indrawing; reduced skin turgor; and bulging fontanelle.

Children exhibiting any of the following symptoms or signs are considered at least intermediate-risk for serious illness: pallor of skin, lips or tongue reported by parent or caregiver; abnormal response to social cues; absence of a smile; waking only with prolonged stimulation; decreased activity; nasal flaring; dry mucous membranes; poor feeding in infants; reduced urine output; and rigors.

Children displaying any of the following symptoms or signs are classified as low-risk for serious illness: normal color of skin, lips, and tongue; normal response to social cues; contentment and smiles; staying awake or quickly awakening; strong normal cry or absence of crying; normal skin and eyes; and moist mucous membranes.

To summarize, children with fever and any symptoms or signs in the red column are considered high-risk, while those with fever and any symptoms or signs in the amber column (but none in the red column) are considered intermediate-risk. Children with symptoms and signs in the green column (and none in the amber or red columns) are classified as low-risk.

For more information, you can refer to the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.