• Local skin involvement after direct contact with spores or bacilli
• Localized itching followed by 1) papular lesion that turns vesicular and 2) subsequent development of black eschar within 7–10 days of initial lesion

• Usually <1 week; may be prolonged for weeks (up to 2 months)

• Non-specific symptoms such as low-grade fever, nonproductive cough, malaise, fatigue, myalgias, profound sweats, chest discomfort (upper respiratory tract symptoms are rare)
• Maybe rhonchi on exam, otherwise normal
• Chest X-ray:
  • mediastinal widening
  • pleural effusion (often)
  • infiltrates (rare)

• 1–5 days after onset of initial symptoms
• May be preceded by 1–3 days of improvement
• Abrupt onset of high fever and severe respiratory distress (dyspnea, stridor, cyanosis)
• Shock, death within 24–36 hours

• Usually 1–7 days

• Nausea, anorexia, vomiting, and fever progressing to severe abdominal pain, hematemesis, and diarrhea that is almost always bloody
• Acute abdomen picture with rebound tenderness may develop.
• Mesenteric adenopathy on computed tomography (CT) scan likely. Mediastinal widening on chest X-ray has been reported

• 2–4 days after onset of symptoms, ascites develops as abdominal pain decreases.
• Shock, death within 2–5 days of onset

• Usually 1–7 days

• Fever and marked unilateral or bilateral neck swelling caused by regional lymphadenopathy
• Severe throat pain and dysphagia
• Ulcers at the base of the tongue, initially edematous and hyperemic

• Ulcers may progress to necrosis
• Swelling can be severe enough to compromise the airway

Lassa fever is an acute viral illness of one to four weeks duration caused by Lassa virus, a member of the arenavirus family of viruses. The disease was first described in the 1950s, although the virus was not isolated until 1969. Consequences range widely in severity, from asymptomatic infection without illness to extremely severe illness which may have a fatal outcome.

Clinical illness

• In clinical illness the onset is gradual, with fever, malaise, headache, sore throat, cough, nausea, vomiting, diarrhoea, myalgia (painful muscles), and chest and abdominal pain. The fever may be either constant or intermittent with spikes. Inflammation of the throat and eyes is commonly observed.
• In severe cases, hypotension or shock, pleural effusion (fluid in the lung cavity), haemorrhage, seizures, encephalopathy (dysfunction of the brain) and swelling of the face and neck are frequent. Approximately 15% of hospitalized patients die. The disease is more severe in pregnancy, and fetal loss occurs in greater than 80% of cases.
• Hair loss and loss of coordination may occur in convalescence. In addition, deafness occurs in 25% of patients, with only half recovering some function after one to three months. Immunity to reinfection occurs following infection, but the length of this period of protection is unknown.

Diagnosis

• Lassa fever is difficult to distinguish from severe malaria, septicaemia (infections of the bloodstream), yellow fever and other viral haemorrhagic fevers (e.g., Ebola). Inflammation of the throat with white tonsillar patches is an important distinguishing feature.
• Definitive diagnosis requires testing that is available in LRN laboratories.

Incubation period: two to 21 days.

Ebola is often characterized by the sudden onset of fever, intense weakness, muscle pain, headache and sore throat. This is often followed by vomiting, diarrhoea, rash, impaired kidney and liver function, and in some cases, both internal and external bleeding. Laboratory findings show low counts of white blood cells and platelets as well as elevated liver enzymes.

Diagnosis

Specialized laboratory tests on blood specimens detect specific antigens and/or genes of the virus. Antibodies to the virus can be detected, and the virus can be isolated in cell culture.

Incubation period. 3 to 9 days.

Susceptibility. All age groups are susceptible to infection, but most cases have occurred in adults. Prior to the present outbreak in Angola, paediatric cases were considered extremely rare. In the largest outbreak previously recorded, which occurred in the Democratic Republic of Congo from late 1998 to 2000, only 12 (8%) of the cases were under the age of 5 years.

Clinical features. Illness caused by Marburg virus begins abruptly, with severe headache and severe malaise. Muscle aches and pains are a common feature.

A high fever usually appears on the first day of illness, followed by progressive and rapid debilitation. A severe watery diarrhoea, abdominal pain and cramping, nausea, and vomiting begin about the third day. Diarrhoea can persist for a week. The appearance of patients at this phase has been described as showing “ghost-like” drawn features, deep-set eyes, expressionless faces, and extreme lethargy. In the 1967 European outbreak, a non-itchy rash was a feature noted in most patients between days 2 and 7 after symptom onset.

Many patients develop severe haemorrhagic manifestations between days 5 and 7, and fatal cases usually have some form of bleeding, often from multiple sites. Findings of fresh blood in vomitus and faeces are often accompanied by bleeding from the nose, gums, and vagina. Spontaneous bleeding at venipuncture sites can be particularly troublesome. During the severe phase of illness, patients have sustained high fevers. Involvement of the central nervous system can result in confusion, irritability, and aggression. Orchitis has been reported occasionally in the late phase of disease (day 15).

In fatal cases, death occurs most often between 8 and 9 days after symptom onset, usually preceded by severe blood loss and shock.

The disease is caused by the yellow fever virus, which belongs to the flavivirus group. In Africa there are two distinct genetic types (called topotypes) associated with East and West Africa. South America has two different types, but since 1974 only one has been identified as the cause of disease outbreaks.

Symptoms

The virus remains silent in the body during an incubation period of three to six days. There are then two disease phases. While some infections have no symptoms whatsoever, the first, "acute", phase is normally characterized by fever, muscle pain (with prominent backache), headache, shivers, loss of appetite, nausea and/or vomiting. Often, the high fever is paradoxically associated with a slow pulse. After three to four days most patients improve and their symptoms disappear.

However, 15% enter a "toxic phase" within 24 hours. Fever reappears and several body systems are affected. The patient rapidly develops jaundice and complains of abdominal pain with vomiting. Bleeding can occur from the mouth, nose, eyes and/or stomach. Once this happens, blood appears in the vomit and faeces. Kidney function deteriorates; this can range from abnormal protein levels in the urine (albuminuria) to complete kidney failure with no urine production (anuria). Half of the patients in the "toxic phase" die within 10-14 days. The remainder recover without significant organ damage.

Yellow fever is difficult to recognize, especially during the early stages. It can easily be confused with malaria, typhoid, rickettsial diseases, haemorrhagic viral fevers (e.g. Lassa), arboviral infections (e.g. dengue), leptospirosis, viral hepatitis and poisoning (e.g. carbon tetrachloride). A laboratory analysis is required to confirm a suspect case. Blood tests (serology assays) can detect yellow fever antibodies that are produced in response to the infection. Several other techniques are used to identify the virus itself in blood specimens or liver tissue collected after death. These tests require highly trained laboratory staff using specialized equipment and materials.