Infectious disease

2 Infectious disease







Fever of unknown origin (FUO)


One definition of a fever of unknown origin is ‘a fever persisting for more than 2 weeks, with no clear diagnosis despite intelligent and intensive investigation’. The definition of FUO has also been refined to include classical FUO, nosocomial FUO, neutropenic FUO and HIV-related FUO.


The causes of FUO, when determined, are infections (20–40%), e.g. endocarditis, TB, Lyme disease; connective tissue disease, e.g. polymyalgia (15–20%); malignancy, e.g. lymphoma (10–30%); and miscellaneous (e.g. drugs).





Systemic multi-system infections



Sepsis


Sepsis is a leading cause of death worldwide and is usually the result of an overwhelming bacterial infection. Most infections, whether bacterial, fungal or viral, initiate a systemic inflammatory response with the release of vasodilatory and pro-inflammatory substances, including cytokines, histamine and prostaglandins. This results in endothelial damage, capillary leak and vasodilatation, causing tissue hypoperfusion. Additionally, the coagulation pathway is activated by a number of cytokines, resulting in microthrombi and further tissue ischaemia. The mortality rate for severe sepsis remains about 30%.




Management


Sepsis and septic shock should be treated urgently, as should the bacterial cause of the infection.











Meningococcal septicaemia


Neisseria meningitidis is found worldwide. There are five major serogroups. The organism is carried asymptomatically in the nasopharynx of 5–20% of the general population. Invasion into the bloodstream (septicaemia-causing disease) depends on both host and bacterial factors.


Presentation is with the classic triad of headache, fever and neck stiffness, though this is not always the case (p. 54). Septicaemia causes septic shock with fever, myalgia and hypotension, and may be accompanied by a petechial or haemorrhagic rash. The case fatality rate is approximately 10%.


N.B. If not treated immediately, patients can deteriorate rapidly, with shock, disseminated intravascular coagulation, multi-organ failure and death.





Malaria


Malaria in humans is caused by Plasmodium falciparum (most severe form), Plasmodium vivax, Plasmodium ovale, Plasmodium malariae or rarely Plasmodium knowlesi, which are transmitted by the Anopheles mosquito. P. vivax and P. malariae may recur after many years, but P. falciparum and P. malariae do not recur, although individuals may be reinfected. P. falciparum causes a potentially fatal malaria that results in about 1–2 million deaths annually, most in children in sub-Saharan Africa. The other causes of malaria are very rarely fatal and may be regarded as the benign malarias.




Diagnosis






P. falciparum infection causes about 200 million infections worldwide annually. WHO advises that fever occuring in a traveller one week or more after entering a malaria risk area and up to three months after departure is a medical emergency because of the mortality associated with P. falciparum. Cases have been reported up to 5 years after leaving a malarial area. Three blood films should be performed. Falciparum malaria is divided into severe and uncomplicated forms.


Severe malaria can present differently in adults and children, but may be defined as the presence of the following features:









The case fatality rate of severe malaria remains between 15 and 30%, despite adequate antiparasitic treatment and good supportive management.




Management of severe falciparum malaria (Box 2.2)









Management of non-falciparum malaria


Non-falciparum malarias can be treated with oral chloroquine 600 mg, then 300 mg after 8 hours, then 300 mg daily for 2 days. There is some reported chloroquine-resistant malaria in Papua New Guinea and treatment can be with riamet or malarone (dosages in Table 2.2). P. vivax and P. ovale have hypnozoites that may persist and cause a recurrence of infection many years later. Patients with vivax or ovale infection should receive primaquine 15 mg daily for 2–3 weeks following successful treatment, to eradicate hepatic hypnozoites and prevent relapse. Anyone who is about to receive primaquine should have their glucose-6-phosphate dehydrogenase (G6PD) status checked, as primaquine use is associated with haemolysis in patients with G6PD deficiency (p. 216). WHO guidelines www.who.int/topics/malaria/en.







Brucellosis


Brucellosis is a zoonosis and nearly all human infections result from direct or indirect exposure to animals. Farmers, veterinarians and abattoir workers are particularly at risk. Spread is following direct contact with infected animals or by the consumption of unpasteurized dairy products from cows, goats or sheep. The pathogens are members of the genus Brucella: in humans usually B. abortus, B. melitensis and B. canis. Brucellosis has a worldwide distribution, although it has been eliminated from the UK. It is especially common in the Mediterranean, India and the Arabian Peninsula.








Lyme disease


Lyme disease is found in North America, Europe and Asia, and is caused by infection with the spirochaete Borrelia burgdorferi, of which there are several genomic species. It is a zoonosis transmitted to man by ixodid ticks, the main animal reservoir being deer or occasionally other mammals. Infections usually occur after visiting woodland.


There are three stages of Lyme infection:








Visceral leishmaniasis


Visceral leishmaniasis (kala-azar) is caused by Leishmania donovani, L. infantum or L. chagasi, and is present in India, Asia, Africa, the Mediterranean and South America. In central India, humans are the main host and the disease occurs in epidemics. In most other areas, it is a zoonosis; the main animal reservoirs are dogs and foxes, although in Africa it is carried by rodents. Visceral leishmaniasis is a common opportunistic infection of advanced HIV disease in Mediterranean coastal regions.







Epstein–Barr virus (EBV)


This herpes virus commonly causes infections, mainly in adolescents and young adults worldwide. It is probably transmitted in saliva and by aerosol.






Skin and soft-tissue infections


Skin infections result in a number of different conditions. The most common organisms causing skin infections are group A streptococci and Staphylococcus aureus.








Meticillin-resistant Staph. aureus (MRSA)


The mec-A gene in Staph. aureus makes it resistant to meticillin, oxacillin, flucloxacillin and nearly all other β-lactam antibiotics. The incidence of MRSA has increased over the last 25 years and in some hospitals more than 50% of Staph. aureus are MRSA; the prevalence of community-acquired MRSA is increasing.


Like meticillin-sensitive Staph. aureus (MSSA), MRSA is usually a harmless skin colonizer, particularly in hospital inpatients. However, both can cause a variety of invasive infections, e.g. soft-tissues infections, bacteraemias, pneumonias and line infections. The case fatality rate of invasive MRSA infections is greater than that of MSSA. Eradication of MRSA carriage is possible, though sometimes difficult. Isolation of patients, strict hand washing, good IV catheter care and other infection control procedures should be observed. Control of the use of antibiotics in hospitals and good infection control policies are vital to prevent spread.


Community-acquired MRSA (CA-MRSA) may have different resistance profiles to hospital strains (often retaining sensitivities) as regards tetracycline, clindamycin and co-trimoxazole. It often produces the exotoxin Panton–Valentine leucocidin and is an increasingly common cause of soft-tissue infections, particularly in the USA (USA300 strain).






Post-streptococcal syndromes


Strep. pyogenes infections usually cause localized throat or skin infections. However, there are a number of immune-associated, generalized complications of Strep. pyogenes.



Rheumatic fever


This is a multi-system inflammatory disorder, occurring in children and young adults as a result of a pharyngeal infection with a group A streptococcus. It is due to molecular mimicry between cell wall M proteins of some group A streptococcus strains, and cardiac laminin and myosin and synovial membrane. Rheumatic fever is much less common in Western Europe and the USA than in other parts of the world; this may be due in part to the treatment of streptococcal infections, e.g. sore throats. The diagnosis of rheumatic fever is made according to the revised Duckett–Jones criteria. The major criteria are carditis, polyarthritis, chorea, erythema marginatum and subcutaneous nodules, while the minor criteria include fever and arthralgia.












Varicella zoster virus (VZV) infection


Primary infection with VZV is in childhood in Europe and the Americas. In some countries (e.g. in South Asia) transmission is different, with more infections in adults.


The primary infection with VZV causes chickenpox, which almost never occurs again in the same person. Chickenpox is infectious from 2 days before the start of the rash until all the vesicles have crusted. The incubation period of chickenpox is 14–21 days. There is a brief ‘flu-like prodromal illness, which may be absent in the young. A rash then develops, with macules rapidly progressing to vesicles, mainly on the head and trunk. The rash occurs in ‘crops’, with skin lesions in all stages typically present on the body. Eventually, the vesicles crust and heal without scarring. Chickenpox is highly infectious and is spread from infected lesions and by the respiratory route. After recovery, VZV remains latent for life in spinal nerve roots. The illness tends to be more severe in adults, particularly pregnant women, smokers and the immunosuppressed. Complications of chickenpox include pneumonia, bacterial superinfection of skin lesions and meningo-encephalitis. VZV can cross the placenta and infection in pregnancy leads to fetal damage in about 2% of cases, mostly in infections before 20 weeks’ gestation.


Shingles is a secondary reactivation of latent VZV infection in the distribution of one or sometimes two dermatomes. The vesicles of shingles are identical to those in chickenpox. Shingles mainly affects the elderly but can occur at any age. Post-herpetic neuralgia may occur after herpes infection and causes severe debilitating pain. Shingles involving the ophthalmic division of the trigeminal nerve has a high rate of complications. Disseminated shingles infection can occur in the immunosuppressed patients (particularly in late HIV infection), when the rash is seen over many dermatomes and appears similar to chickenpox. Shingles lesions may transmit infection to non-immune individuals.






Respiratory infections



Upper respiratory tract infections










Diphtheria


Diphtheria is caused by pharyngeal or cutaneous infection with toxigenic strains of Corynebacterium diphtheriae and, rarely, toxigenic strains of C. ulcerans. Classical diphtheria presents with a membranous pharyngitis, cervical lymphadenopathy and oedema of the surrounding soft tissues. The membrane, which is not always present, is typically grey, thick and adherent. Laryngeal involvement also occurs, and causes hoarseness and stridor. Nasal diphtheria may present as a bloody nasal discharge. Cutaneous diphtheria is commoner in tropical countries and usually affects the legs. The lesions start as vesicles and progress to form ulcers.







Apr 2, 2017 | Posted by in GENERAL SURGERY | Comments Off on Infectious disease

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