section name header

Information ⬇

Editors

HeliSiikamäki
AnuKantele

Bacterial Diseases in Warm Climates

Essentials

  • A doctor working in non-endemic regions will need to consider the bacterial diseases discussed in this article when working in endemic areas and when treating international travellers or immigrants.
  • Some of the diseases are acute and life-threatening infections.
  • Some of the infections are rare.
  • For example, anthrax can be contracted by handling imported leather and can therefore, in principle, also be found in the industrialised countries, and it is a potential agent for bioterrorism/biological warfare.
  • The diseases are presented in rough order of frequency.

Typhoid fever and paratyphoid fever

Causative agent

  • Typhoid fever is caused by Salmonella enterica, serovar Typhi, and paratyphoid fever by serovars Paratyphi A, B or C (often referred to as S. Typhi and S. Paratyphi).
  • Typhoid and paratyphoid fever are collectively referred to as enteric fever.

Transmission

  • Transmission occurs via a faecal-oral contact.
  • In most cases transmission occurs through food or drink in poor countries with insufficient hygiene conditions, particularly after a lengthy stay in the countryside.

Occurrence and global significance

  • The estimated annual number of cases of typhoid fever is about 20 million and that of paratyphoid fever about 6 million. The annual number of deaths is estimated to be about 150 000.
  • The highest risk of acquiring the disease is in the Indian subcontinent, where the incidence of paratyphoid fever has increased significantly over the last decade, and antimicrobial resistance has rapidly increased.
  • Typhoid fever and paratyphoid fever are notifiable infectious diseases, and the treating physician must report all confirmed cases to the authorities.

Symptoms

  • Enteric fever is an acute febrile disease: fever increases in a stepwise fashion over the first few days, which is followed by sustained high fever.
  • The incubation period is 2-3 weeks (range 3-60 days).
  • The clinical presentations of typhoid and paratyphoid fever are very similar.
  • In addition to fever, other early symptoms include headache, sweating, chills, nausea, loss of appetite and often also dry cough.
  • Gastrointestinal symptoms are not always present, and they generally appear later as pain, constipation, diarrhoea or vomiting. Abdominal symptoms may at least partially be due to other simultaneously contracted intestinal pathogens.
  • Hepatomegaly and splenomegaly as well as relative bradycardia may develop.
  • About one third of patients develop transient skin changes (rose spots).
  • Complications may include intestinal haemorrhage and bowel perforation, sometimes encephalopathy, spleen abscess, endocarditis, arthritis or cholecystitis.

Diagnosis

  • Based on blood cultures.
  • Faecal culture: especially during the second week of illness bacteria may also be detected in the faeces.
  • If antimicrobial medication has already been started, a bacterial culture may also be done on a bone marrow aspiration in which case the sensitivity is about 90%. The bacteria may also be cultured from the rose spot skin manifestations.
  • Typical findings in the blood tests are leucopenia, thrombocytopenia and increased aminotransferase concentrations. CRP is usually only slightly increased.

Treatment

  • Typhoid fever is always treated in a hospital.
  • Treatment consists of intravenous ceftriaxone for 14 days, adult dose 2 g once daily. Azithromycin should also be added, especially for patients who have travelled in the Indian subcontinent.
  • The majority of S.Typhi and S. Paratyphi strains in the Indian subcontinent are resistant to fluoroquinolones; resistance has also increased elsewhere.

Prognosis

  • A chronic carrier status develops in about 2-5% of patients, less frequently in travellers than in those originating from endemic regions, in whom complications are also noticeably more common.
  • In endemic regions, the mortality rate in untreated disease is 30%.
  • Travellers seek medical assistance quickly; the mortality rate is estimated to be 0.4%.

Prevention Vaccines for Preventing Typhoid Fever

  • Two vaccines against typhoid fever are available to travellers: an injectable vaccine containing the Vi capsular polysaccharide from S. Typhi and an oral vaccine containing live attenuated bacteria of the S. Typhi Ty21a strain. Their prophylactic efficacy is similar (about 60-70%). A new injectable combined vaccination against hepatitis A and typhoid fever, containing capsular polysaccharide Vi from S. Typhi, entered the market in 2018.
  • No vaccine is available against paratyphoid fever. However, the oral typhoid vaccine has been shown to have some effectiveness also against paratyphoid fever (at least against S. Paratyphi B), the injectable vaccine does not share this property.

Rickettsioses or spotted fevers

Causative agent

  • Rickettsiae are intracellular microbes that invade the intima of blood vessels causing vasculitis.
  • Several species of rickettsia are known to cause human disease. Rickettsia prowazekii causes epidemic or louse-borne typhus, R. typhi (moseri) causes endemic (or murine) or flea-borne typhus, R. conorii causes Mediterranean spotted fever, R. africae causes African tick-bite fever, R. ricketsii causes Rocky Mountain spotted fever, and Orientia tsutsugamushi causes scrub typhus.

Occurrence

  • Epidemic typhus occurs particularly in Africa, South and Central America and Asia. It spreads, for example, in refugee camps and anywhere in crowded living conditions where the inhabitants are clothed. Epidemics usually appear in the winter.
  • Endemic typhus occurs in Africa, Asia and Europe. Other rickettsioses often occur in limited endemic areas. Mediterranean spotted fever occurs in countries around the Mediterranean, Africa, India, around the Black Sea and Russia, African spotted fever occurs on the African continent, Rocky Mountain spotted fever in North, Central and South America, and scrub typhus in Asia, particularly in Southeast Asia. Cases of perimyocarditis caused by R. helvetica and leading to sudden death have been described in Sweden.

Transmission

  • The infection is spread by arthropods: body louse (R. prowazekii), flea (R. typhi) or tick (R. conorii, R. africae, R. ricketsii, R. helvetica etc, i.e. the spotted fever group) or soft-bodied ticks (Orientia tsutsugamushi).

Global significance

  • Epidemic spotted fever spreads in conditions where hygiene is poor, and it has been estimated to have killed more people in the course of history than all the wars put together.
  • Significant causative agents of febrile diseases in Southeast Asia
  • Some rickettsioses are associated with significant mortality if left untreated.

Symptoms

  • The incubation period is usually less than 2 weeks, 2 days at the shortest.
  • Acute high fever, myalgia, nausea and severe headache are typical symptoms.
  • Characteristic maculopapular rash and/or purpura appears in most rickettsioses within 3-7 days. However, it can also be absent. In some rickettsioses the rash may be vesicular, resembling chickenpox.
  • In some tick-borne spotted fevers (e.g. African and Mediterranean spotted fevers) and scrub typhus, the patient may have a necrotic lesion on the skin (”eschar”, ”tache noire”) 1 at the site of the arthropod bite (resembles a cigarette burn).
  • Other possible symptoms
    • Lymphadenopathy, cough, lung infiltrates, conjunctivitis, pharyngitis, nausea, vomiting, abdominal pain, elevated liver enzyme levels, hepatosplenomegaly, CNS symptoms, arrhythmias, myocarditis, proteinuria, renal failure
  • An infection by R.helvetica should be considered in a traveller who develops a febrile illness after a tick bite accompanied by cardiac symptoms or increased liver enzyme concentrations.

Diagnosis

  • Febrile illness (and rash) and/or a ”tache noire” in a person who has stayed in an endemic area and possibly been exposed to a bite from a hard or soft tick, a flea or a louse. Treatment is initiated on the basis of clinical presentation as rapid diagnostic methods are not available in routine use.
  • The blood white cell count is usually normal.
  • In the acute phase the diagnosis is usually clinical. Blood culture samples and other bacteriological samples should be obtained in order to take into account other serious bacterial diseases, and the possibility of malaria is excluded before treatment is started.
  • Specific antibodies (R. conorii antibodies cross react with rickettsiae of the spotted fever group, R. typhi antibodies cross react with R. prowazekii and B. quintana) are often not elevated until after 4-12 weeks of the disease onset. Diagnostic testing for Orientia tsutsugamushi is not widely available.
  • A PCR assay from a ”tache noire” (special arrangement with the laboratory may be needed).

Treatment

  • Doxycycline 100 mg twice daily, continued for at least a few days after the fever has subsided, usually for 7-14 days in total.
  • Consult an infectious disease physician.

Prognosis

  • Varies with different species, usually good. Response to doxycycline is usually quick.
  • Epidemic typhus, Rocky Mountain spotted fever, Mediterranean spotted fever and scrub typhus may be life threatening, particularly if the diagnosis is delayed.

Prevention

  • Avoidance of arthropod bites

Q fever

Causative agent

  • Coxiella burnetii, an intracellular microbe which, unlike rickettsiae, can survive outside the cell and remain viable in a spore form in dry dust for a long time.

Occurrence

  • Occurs globally, especially in cattle farming regions not including North Europe.

Transmission

  • Q fever is a zoonosis.
  • Transmitted to humans mainly via airborne droplets either through contact with the afterbirth, wool, faeces or urine of cattle, goats, sheep or cats, or carried with the wind from the soil. May also be transmitted by unpasteurised milk.

Global significance

  • A common febrile disease, encountered also in Europe.
  • May be underdiagnosed in travellers.

Symptoms

  • Most infections are asymptomatic, or mild, and self-limiting febrile illnesses.
  • The incubation period is usually 2-3 weeks (1-8 weeks).
  • The clinical picture resembles that of influenza: high fever, headache and myalgia and/or pneumonia and/or hepatitis
  • Around one third of patients have clinical or radiological pneumonia, around half have hepatosplenomegaly.
  • Renal complications, carditis and aseptic meningoencephalitis may develop.
  • Five to seven per cent of patients develop chronic Q fever, the most common manifestation of which is cardiac valvulitis, which develops 1-20 years after the acute infection.
  • The risk of chronic Q fever is highest in patients with valvular heart disease, in immunocompromised patients and in pregnant women.
  • The possibility of Q fever should be borne in mind in culture negative endocarditis.

Diagnosis

  • Suspicion: a patient who presents with fever and flu-like symptoms and/or pneumonia and/or hepatitis and who has travelled to an endemic region within the 3 months preceding disease onset, particularly if there is a history of animal contact or ingestion of unpasteurised milk products.
  • Blood white cell count is usually normal, thrombocytopenia may occur, liver enzymes are often raised.
  • Diagnosis is based on antibody determination. Antibody titres often do not rise until 3-4 weeks after the onset of the disease.

Treatment

  • A long course of antimicrobials that should be started within 3 days from the first symptoms. Treatment may prevent the development of a chronic disease. The first-line treatment in acute disease is doxycycline 100 mg twice daily for 2-3 weeks. Fluoroquinolones and macrolides are used as alternatives; their efficacy has not been conclusively shown. Children and pregnant women are prescribed co-trimoxazole.
  • Consult an infectious disease physician.

Prognosis

  • Acute Q fever proves to be fatal in 1-2% of cases. Acute Q fever often resolves spontaneously without treatment but may lead to chronic Q fever.
  • Eradication of chronic Q fever is difficult and relapses are common.

Prevention

  • Avoidance of animal contact and unpasteurised milk products.

Leptospirosis

Causative agent

  • Spirochetes of the Leptospira genus
  • Leptospira interrogans is the most common agent.

Occurrence

  • The disease occurs worldwide.

Transmission

  • Leptospirosis is a zoonosis.
  • The disease is usually transmitted to humans through the skin or mucous membranes by soil or water contaminated by the urine of an infected animal.
  • The bite of an infected animal, handling or eating infected tissues are more rare modes of transmission.

Global significance

  • Fairly common. Occupational transmission is frequent (e.g. fishermen, farmers).
  • The cases of leptospirosis in travellers have increased, one reason being the increased popularity of adventure travel and water sport activities in tropical regions.

Symptoms

  • The incubation period is 2-30 days
  • Subclinical disease is possible, but likely to be rare.
  • Leptospirae cause small vessel vasculitis making it possible for the bacteria to penetrate target organs though the damaged endothelium.
  • Symptoms usually resemble those of influenza, meningitis or hepatitis
  • The course of the disease is often biphasic.
  • Symptoms begin with a high fever which may be accompanied by headache and severe muscle pains, even rhabdomyolysis. Ocular sensitivity to pressure, photophobia and conjunctional suffusion are also common.
  • The febrile phase is followed by a ”secondary phase”, which is characterised by varying organ manifestations. Aseptic meningitis develops in almost half of the patients. Other signs and symptoms that have been described include abdominal pain, vomiting, diarrhoea, confusion, rashes, lymphadenopathy, splenomegaly, carditis, renal insufficiency and haemolysis.
  • In the severe form of the disease (Weil's disease) the symptoms include jaundice, renal insufficiency, haemorrhages and shock.
  • Leucocytosis is a characteristic finding, aminotransferase concentrations are often raised and CK may be high.
  • Potential complications include renal failure requiring dialysis and cardiogenic shock.

Diagnosis

  • Suspicion: a febrile disease with symptoms of influenza, hepatitis or meningitis and a history of contact with fresh water or soil.
  • Diagnosis is based on serology (Leptospira antibodies). The antibody titres do not usually rise until at the end of the second week of illness, and they may remain raised for several years.

TreatmentAntibiotics for Leptospirosis

  • Severe forms of the disease should be treated with intravenous penicillin or ceftriaxone for 7 days, milder forms with oral doxycycline (100 mg twice daily) for 7 days.
    • Antimicrobial treatment is often associated with a Jarisch-Herxheimer (JH) reaction (fever, confusion, tachycardia, an initial pressor response followed rapidly by hypotension).
    • Medical treatment is started in a hospital and the patient should be monitored for at least 24 hours.
    • Consult an infectious disease physician.

Prognosis

  • The mortality is 5-10% in Weil's disease.

Prevention

  • Travellers should be advised to avoid exposure to fresh water in tropical regions. Walking barefoot will also increase the risk. If the risk of exposure is particularly high, 200 mg of doxycycline once a week may be used. However, evidence of its efficacy remains controversial Antibiotic Prophylaxis for Leptospirosis.
  • A vaccine has been developed, but it is not available in all countries. Vaccination has been used in individuals at risk of occupational exposure in endemic areas.

Relapsing fever

Causative agent

  • Epidemic relapsing fever is caused by the spirochete bacteria Borrelia recurrentis.
  • Endemic relapsing fever is caused by other Borrelia species.

Occurrence

  • Epidemic relapsing fever occurs globally among people living in poverty, most frequently in Africa and South America. Endemic relapsing fever occurs in much of the world.

Transmission

  • The epidemic form is transmitted by lice from humans to humans, the endemic form is transmitted by ticks from small mammals to humans.

Global significance

  • Relapsing fever is fairly common. Louse-borne epidemics occur during wars, famine or the mass movement of people.
  • Relapsing fever is rare in travellers.

Symptoms

  • Fever with chills, severe headache, myalgia, arthralgia, photophobia, nausea and dry cough develop after an incubation period of one week. The primary febrile episode lasts for 3-6 days.
  • After an afebrile period lasting for one week the patient experiences relapses each lasting for 2-3 days. In the epidemic form of the disease 1-5 relapses are usual, in the endemic form there are more.
  • At the end of the febrile episode the most common signs and symptoms include splenomegaly, hepatomegaly, jaundice, rashes, cranial nerve palsy, meningitis, hemiplegia, epileptic seizures.
  • The disease may be accompanied by bleeding tendency and petechiae.

Diagnosis

  • Diagnosis can be obtained by a microscopic examination of thick and thin blood smears taken during a febrile episode (Borrelia recurrentis staining, see malaria samples).
  • No specific antibody assays exist, serological cross reactions are possible against the antigens of other spirochete species (syphilis, Lyme borreliosis, spotted fever).

Treatment

  • Doxycycline for 10 days; in the epidemic form a single dose is sufficient in principle.
  • Borrelia recurrentis is also sensitive to beta-lactams, macrolides and possibly to fluoroquinolones.
  • The treatment of severe disease is intravenous ceftriaxone.
  • Antimicrobial treatment is often associated with a Jarisch-Herxheimer (JH) reaction (fever, confusion, tachycardia, an initial pressor response followed rapidly by hypotension).
  • Consult an infectious disease physician.

Prognosis

  • Mortality in the epidemic form is 4-40%, in the endemic form 2-5%.

Prevention

  • Improving general hygiene, delousing, avoidance of tick bites

Brucellosis

Causative agent

  • Brucellae are Gram-negative very short rod-shaped bacteria (coccobasilli). Of these, B. melitensis, B. abortus, B. canis and B. suis can infect humans.

Occurrence

  • Most prevalent among inhabitants of cattle farming regions in the Middle East, Central Asia, Africa, the Indian subcontinent, Mediterranean countries as well as in Central and South America.

Transmission

  • Brucellosis is a zoonosis.
  • The most important route of infection is milk, especially untreated goat's milk and its by-products.
  • Brucellosis may also be contracted from infected animals via airborne aerosols, especially when the animal is giving birth.

Global significance

  • Used to be fairly common. Incidence has decreased along with pasteurisation of milk.

Symptoms

  • The majority of infections are subclinical or only have mild symptoms and resolve spontaneously within 2-3 weeks.
  • The incubation period is 2-4 weeks, but may occasionally be considerably longer.
  • Symptoms characteristically include prolonged undulating fever, headache, back pain, myalgia, arthralgia, dry cough and systemic symptoms.
  • Typical findings include inflammation of joints and bones as well as enlarged liver, spleen and lymph nodes.
  • Anaemia, lymphocytopenia and raised liver enzymes are common.
  • A minority of patients will develop complications, such as endocarditis, meningitis, arthritis or spondylodiscitis.
  • Brucellosis can be classified as acute (duration < 1 month), relapsing (< 6 months from the previous episode) or chronic (duration > 6 months).

Diagnosis

  • Blood cultures (positive in 40-70% of cases), bacterial culture from bone marrow (positive in 90% of cases), purulent material or tissues (synovial fluid, lymph nodes, CSF)
  • If brucellosis is suspected, the laboratory staff should be alerted beforehand since Brucella bacteria require a special technique, a longer than normal culture time (3-6 weeks) and appropriate protection for the laboratory staff due to the risk of transmission via airborne aerosols.
  • Brucella antibodies
    • As there is potential cross-reactivity with the lipopolysaccharide of Yersinia enterocolitica serotype O:9, both antibodies should be determined at the same time.

TreatmentAntibiotics for Treating Human Brucellosis

  • Combination treatment since the disease recurs easily (10-40%) if only one antimicrobial is used.
  • Doxycycline combined with either an aminoglycoside or rifampicin or a combination of the three. In children, co-trimoxazole and an aminoglycoside.
  • Severe infections are treated with a combination of several antimicrobials.
  • The treatment duration is at least 6 weeks, in complicated cases (spondylitis, endocarditis, meningitis) 3-6 months.
  • Endocarditis is usually an indication for valve surgery.
  • A relapsed case is one that reoccurs within 6 months. Most commonly this happens due to the patient's poor compliance with the long course of antimicrobials.
  • Consult an infectious disease physician.

Prognosis

  • Untreated disease is associated with 2% mortality.

Prevention

  • Avoidance of unpasteurised milk products.
  • Mass vaccination of animals in endemic regions.

Melioidosis

Causative agent

  • Burkholderiapseudomallei, Gram-negative rod-shaped bacteria

Occurrence

  • Endemic in parts of South and Southeast Asia as well as northern Australia.
  • Melioidosis is most prevalent in Northeast Thailand, where the seroprevalence in the population is approximately 60-70% and B. pseudomallei is accountable for 20% of all blood culture findings.

Transmission

  • Transmission occurs through direct contact with soil and surface water, particularly in the presence of broken skin.
  • Chronic diseases, such as diabetes, chronic lung diseases as well as renal and hepatic insufficiency predispose a person to melioidosis, but also a generally health person may contract the disease.

Global significance

  • In endemic regions melioidosis is a common cause of bacteraemia and pneumonia.
  • Melioidosis is possible in travellers returning from Thailand.

Symptoms

  • The incubation period is usually 10-14 days (range 1 day-several years).
  • The clinical picture may include
    • localised skin infection
    • acute pulmonary infection
    • acute sepsis
    • disseminated infection.
  • Based on the incubation period and duration, the clinical picture can be
    • an acute infection
    • a subacute infection
    • a chronic infection.
  • In some cases, the clinical presentation may resemble that of tuberculosis.
  • The bacteria may remain in the body and re-activate even after several decades.
  • In travellers the most common form is localised skin infection, which manifests as an infected ulcer or as an abscess and fever.
  • Sepsis and severe pneumonia with cavitary lesions may quickly prove to be fatal.

Diagnosis

  • Melioidosis should be suspected in travellers returning from endemic regions, who present with a purulent skin infection or a serious septic bacterial infection, particularly if the clinical picture is associated with severe pneumonia.
  • Diagnosis is based primarily on blood cultures or a bacterial culture of urine, sputum, skin lesion or abscess.
  • The receiving laboratory should be informed if melioidosis is suspected.
  • An antibody assay is available.

Treatment

  • The initial antimicrobials used routinely in sepsis are not effective against melioidosis.
  • The antibiotics used are intravenous ceftazidime or meropenem for 10-14 days.
  • After the intravenous therapy is completed, antimicrobial therapy is continued using oral co-trimoxazole alone or combined with doxycycline for a further 3-6 months.
  • An infectious disease physician should always be consulted.

Prognosis

  • The mortality rate in bacteraemic pneumonia is about 30%.

Prevention

  • No vaccine against melioidosis is available.
  • Prevention consists of cleaning and protecting skin breaks and wounds as well as avoiding contact with the soil and stagnant water.

Leprosy

Causative agent

  • Mycobacterium leprae

Occurrence

  • Endemic in several developing countries. Since 1995 the prevalence has decreased by 90%. WHO has guaranteed free treatment for everyone.

Transmission

  • Spread by droplet infection between humans. Usually a long-term near contact with the disease carrier is required.

Global significance

  • A significant health problem in endemic areas

Symptoms

  • Incubation period 2-12 years
  • Skin changes
    • Skin areas that are lighter in colour than the surrounding areas and where sensation and sweating have decreased
    • Large areas of thickened skin and nodules
  • Palpable, thickened nerve trunks and peripheral paralyses
    • Injuries of fingers and toes resulting from of neuropathy and neuropathy-related trauma
  • Lepra reactions: immunological reactions that are often related to the treatment start. Symptoms include, among others, fever, iritis, neuritis.

Diagnosis

  • Staining for mycobacteria from skin smears (slit-skin smears taken from ear lobules) or from skin biopsy. Mycobacterium leprae will not grow in mycobacterial culture.

Treatment Corticosteroids for Nerve Damage in Leprosy, Decompressive Surgery for Treating Nerve Damage in Leprosy, Interventions for Erythema Nodosum Leprosum

Prognosis

  • The prognosis is good if treatment is started early.

Prevention Vaccination Against Mycobacterium Leprae

Anthrax

Causative agent

  • The bacillus Bacillus anthracis

Occurrence

  • Animal anthrax is encountered, among other regions, in South and North America, the Caribbean Islands, East and South Europe, the Middle East, Asia and Africa.

Transmission

  • Anthrax is transmitted from animals to humans (a zoonosis). The disease occurs in herbivores and is occasionally transmitted to humans.
  • The domestic animal reservoirs are cattle, sheep, goats, horses and pigs.
  • Anthrax spores can survive for many years in dried or otherwise treated animal skins and hides as well as in the soil.
  • Humans can be infected through skin, respiratory tract or digestive tract.
    • Cutaneous anthrax can be contracted through skin contact with, for example, a diseased animal's tissues, wool or hide or with contaminated soil.
    • Pulmonary anthrax can be contracted through inhaling spores, for example, when handling goat hair.
    • Gastrointestinal anthrax can be contracted through eating contaminated meat.
  • A deliberate release of anthrax spores can be used in biological warfare or bioterrorism. In this case the clinical picture would be that of either pulmonary or cutaneous anthrax.
  • Anthrax does not spread from human to human.

Global significance

  • An animal disease, transmission to humans is rare.
  • A potential agent for biological warfare and bioterrorism.

Symptoms

  • Cutaneous anthrax is the most common type. The incubation period is usually 2-5 days. The disease begins with a papule that turns into a vesicle. The vesicles merge and rupture. Seven to ten days after disease onset a 1-3 cm sized black and painless ulcer develops on the site. The ulcer develops a scab that falls off after 1-2 weeks leaving a scar. If left untreated, the infection may spread and become generalised.
  • Inhalation of the bacterial spores causes a biphasic disease, which starts with flu-like symptoms after an incubation period of 1-5 days. This is followed in 2-5 days by severe, often fatal mediastinitis.
  • Gastrointestinal anthrax is rare. Symptoms include vomiting and fever, and at a later stage abdominal pain, haematemesis and malaena; the clinical presentation may resemble acute intestinal bleeding.

Diagnosis

  • Suspicion
    • Acute febrile disease in a traveller arriving from an endemic region who has been in contact with animals or animal products and presents with the above clinical symptoms.
    • A deliberate release of the anthrax bacteria is suggested by symptoms consistent with pulmonary or cutaneous anthrax.
      • Whenever anthrax is suspected, local authorities must be immediately contacted.
  • Blood cultures × 2, bacterial staining and culture, PCR either from a skin lesion, sputum or faeces depending on the type of disease, antibody assay.
  • The laboratory personnel must be alerted beforehand.
  • The request form must include a warning of a suspected case of anthrax and a ”danger of infection” sticker.
  • A patient with suspected anthrax need not be nursed in isolation. All waste is considered as infectious.
  • Antimicrobial therapy must be started as soon as possible. The first-line treatment is intravenous penicillin or ciprofloxacin. The duration of treatment is approximately 60 days, in cutaneous anthrax 7-10 days.
  • Anthrax is a notifiable disease. All confirmed and highly suspected cases must be reported to the appropriate authorities.

Prognosis

  • Cutaneous anthrax: mortality 5-20% in untreated cases, and very low with antimicrobials
  • Pulmonary anthrax: mortality 90-100% even if treated
  • Gastrointestinal anthrax: mortality 25-100% in untreated cases

Exposure (a suspicion of deliberate release of anthrax spores)

  • The evaluation of the probability of exposure and the decision on taking samples and treating exposed persons with antimicrobials are made in cooperation with infection specialists, health authorities and other authorities in charge of national safety issues.
  • Any area that is suspected of being contaminated by bacterial spores is closed. A list is compiled of all individuals within the area, and appropriate officials ensure that samples are taken from suspected sources of infection.
  • A person exposed to anthrax spores is not infectious and isolation is not necessary, but decontamination is necessary through washing and changing clothing.
  • If the above authorities evaluate the exposure to be real, prophylactic antimicrobials must be started as soon as possible in all exposed individuals; first-line treatment is ciprofloxacin. If the exposure is confirmed, the treatment is continued for 60 days.

Prevention Vaccinations for Preventing Anthrax

  • Surveillance of infections in animals, burning carcasses of all infected animals.
  • A vaccine has been developed, but it is not available in all countries.

Plague

Causative agent

  • Yersinia pestis bacteria

Occurrence

  • Occurs fairly rarely globally. About 200 plague cases are reported annually in Africa, Asia and South America. Plague is also encountered in the United States.

Transmission

  • Plague is a zoonosis.
  • The carriers of plague are rodents, especially rats.
  • The infection is spread by the bites of fleas.
  • Pneumonic plague can be transmitted from person to person via airborne droplets.

Global significance

  • Historically plague has played a major part as the cause of mass epidemics.
  • Plague could in principle be used as an agent for bioterrorism. In such a case, the release would likely be in the form of airborne droplets.

Symptoms

  • After an incubation period of 2-8 days bubonic plague manifests itself as enlarged lymph nodes in the groin, axilla or neck as well as high fever.
  • An inhalation of plague bacteria may result in pneumonia, which is usually fatal (pneumonic plague; may also develop as a complication in bubonic plague).

Diagnosis

  • Clinical suspicion must prompt immediate treatment.
  • Bacterial staining and culture

Treatment

  • Streptomycin or gentamicin is the first-line treatment.
  • Doxycycline and probably fluoroquinolones are also effective.
  • Consult an infectious disease physician.

Prognosis

  • Mortality in bubonic plague is approximately 50% in untreated cases, up to 100% in pneumonic plague and septicaemic plague.
  • Antimicrobial therapy is effective only when introduced early in the disease, in which case mortality is approximately 5%.

Prevention Vaccines for Preventing Plaque

  • Eradication of rodent reservoir hosts
  • No effective vaccine has been developed.

Disease-specific pages by the ECDC and CDC

References

  • Leshem E, Meltzer E, Schwartz E. Travel-associated zoonotic bacterial diseases. Curr Opin Infect Dis 2011;24(5):457-63. [PubMed]
  • Wain J, Hendriksen RS, Mikoleit ML ym. Typhoid fever. Lancet 2015;385(9973):1136-45.
  • Kariuki S, Gordon MA, Feasey N et al. Antimicrobial resistance and management of invasive Salmonella disease. Vaccine 2015;33 Suppl 3():C21-9. [PubMed]
  • Waddington CS, Darton TC, Pollard AJ. The challenge of enteric fever. J Infect 2014;68 Suppl 1():S38-50. [PubMed]
  • Blanton LS. Rickettsial infections in the tropics and in the traveler. Curr Opin Infect Dis 2013;26(5):435-40. [PubMed]
  • Jensenius M, Fournier PE, Raoult D. Rickettsioses and the international traveler. Clin Infect Dis 2004;39(10):1493-9. [PubMed]
  • Delord M, Socolovschi C, Parola P. Rickettsioses and Q fever in travelers (2004-2013). Travel Med Infect Dis 2014;12(5):443-58. [PubMed]
  • Million M, Thuny F, Richet H et al. Long-term outcome of Q fever endocarditis: a 26-year personal survey. Lancet Infect Dis 2010;10(8):527-35. [PubMed]
  • Dupouey J, Faucher B, Edouard S et al. Human leptospirosis: an emerging risk in Europe? Comp Immunol Microbiol Infect Dis 2014;37(2):77-83. [PubMed]
  • Forbes AE, Zochowski WJ, Dubrey SW et al. Leptospirosis and Weil's disease in the UK. QJM 2012;105(12):1151-62. [PubMed]
  • Dean AS, Crump L, Greter H et al. Clinical manifestations of human brucellosis: a systematic review and meta-analysis. PLoS Negl Trop Dis 2012;6(12):e1929. [PubMed]
  • Solís García del Pozo J, Solera J. Systematic review and meta-analysis of randomized clinical trials in the treatment of human brucellosis. PLoS One 2012;7(2):e32090. [PubMed]
  • Wiersinga WJ, Currie BJ, Peacock SJ. Melioidosis. N Engl J Med 2012;367(11):1035-44. [PubMed]
  • Dance D. Treatment and prophylaxis of melioidosis. Int J Antimicrob Agents 2014;43(4):310-8. [PubMed]
  • White C, Franco-Paredes C. Leprosy in the 21st century. Clin Microbiol Rev 2015;28(1):80-94. [PubMed]
  • Prentice MB, Rahalison L. Plague. Lancet 2007;369(9568):1196-207. [PubMed]

Evidence Summaries ⬆