Microbiology II Flashcards
Fungal infections
Fungal infections cause three types of disease:
- infections (mycoses)
- mycotoxicoses
- allergic reactions.
Infections (mycoses)
1. Superficial infections. The commonest encountered surgically is infection of the mucous membrane with yeasts (thrush). Infections of keratinized tissues of skin, nail and hair occur. Abnormalities of toe nails may be caused by fungi.
- Subcutaneous infections may occur as the result of traumatic implantation of spores leading to local disease with tissue destruction and sinus formation. Such infections are rare in the UK but are more common in tropical regions.
Yeasts: Candida
Candida spp are involved in invasive mycoses. Candida spp, especially Candida albicans are isolated from blood cultures with increasing frequency. Infection is usually endogenous but cross-infection may occur.
Patients at risk include:
• premature babies;
• adults with debilitating diseases, e.g. diabetes;
• immunocompromised;
• AIDS;
• transplant patients on immunosuppressive drugs;
• malignancy, especially leukaemia, lymphoma;
• patients on long term broad spectrum antibiotics
or cytotoxic drugs; and
• patients undergoing surgical procedures.
Yeasts: Candida: Clinical
Clinical features
Infection (candidiasis) depends on the host’s suscep- tibility. Minor susceptibility leads to mild, superficial infections, whilst more serious susceptibility leads to deep invasive infections.
Superficial infections include:
• mucous membranes, e.g. thrush – white patches on buccal mucosa, vagina or oesophagus;
• skin, e.g. red weeping areas where skin is moist, e.g. intertrigo in obese patients; and
• deep, e.g. endocardium, heart valves, eye, meninges, kidney, liver, bone.
Yeasts: Candida: Treatment
Superficial infections
Topical preparations, e.g. nystatin or amphoteracin or an imidazole, e.g. miconazole or clotrimazole.
Systemic infections
Intravenous therapy is required, e.g amphoteracin B, flu- cytosine or a combination of both. Oral fluconazole or itraconazole may be used in mucosal or systemic infec- tions. They may also be used prophylactically in suscep- tible patients, e.g. neutropenic or immunosuppressed.
Other yeast infections are rare in surgical patients.
Filamentous fungi
Dermatophytes
These cause infection of the keratinised tissue of skin, nails and hair, e.g. tinea, ringworm.
Aspergillus
Invasive aspergillosis is a well recognised complica- tion of prolonged immunosuppression and is a main cause of death in patients undergoing allogeneic bone marrow transplants. Aspergillus fumigatus is the main pathogen. Aspergillus spp cause a variety of clinical pictures as follows:
- Allergic bronchopulmonary aspergillosis. Inhaled spores cause hypersensitivity reactions, e.g. type I (asthma), type III (extrinsic alveolitis).
- Aspergilloma. Fungal balls grow in existing lung cavities due to TB, bronchiectasis, sarcoid and malignancy.
• Invasive aspergillosis. Usually seen in the immuno- compromised with pneumonia and later spreads to brain, kidneys and heart. Treatment of invasive aspergillosis is with intravenous amphotericin B, caspofungin or voriconazole. Mortality is
high reaching 90% in patients with persistent neutropenia.
Mould pathogens
Pneumocystis carinii
This is a predominant cause of pneumonia in HIV- infected individuals. It may also occur in immunosup- pressed transplant patients. It is usually the result of reactivation of latent infection. A severe pneumonia with progressive dyspnoea and respiratory failure results. Chest x-ray reveals diffuse infiltrates with a ‘white out’ of the lungs. Diagnosis is via demonstra- tion of the characteristic cysts in bronchial aspirates, bronchial lavage or lung biopsy. Treatment is by co-trimoxazole or pentamidine.
Classification of wounds (1 & 2)
Wounds may be classified by their potential for infection:
- clean: an operation carried out through clean
non-infected skin under sterile conditions where the GI tract GU tract, or respiratory tract are not breached, e.g. hernia repair, varicose vein surgery; the risk of wound infection should be less than 2%; - clean contaminated: an operation carried out under sterile conditions with breaching of a hollow viscus other than the colon, where contamination is minimal, e.g. cholecystectomy; the risk of wound infection should be less than 8%;
Classification of wounds (3 & 4)
- contaminated: an operation carried out where contamination has occurred, e.g. by opening the colon, an open fracture, or animal or human bites; the risk of wound infection is around 12%; and
- dirty: an operation carried out in the presence
of pus, or a perforated viscus, e.g. perforated appendicitis, faecal peritonitis; the risk of wound infection is 25%.
Hospital-acquired infections
Hospital-acquired infections, or nosocomial infections occur in about 10% of hospitalised patients. The com- monest are UTIs, wound infections, lower respiratory tract infections, and skin and soft tissue infections. Present-day pathogens are often resistant to antibiot- ics, a major problem being methicillin-resistant Staph. aureus (MRSA). Predisposition to hospital-acquired infection includes:
• age – the extremes of life;
• susceptible patients, e.g. immunosuppressed,
diabetic, those with prosthetic implants; and
• modes of treatment, e.g. intravenous lines,
indwelling catheters, etc.
The origin of bacterial infection may be divided into two main sources:
• endogenous – with patient’s normal flora; and
• exogenous – from other people or objects in the
environment.
Endogenous infection
This occurs where the organism is carried by the patient either as part of the normal flora or ‘replacement’ flora, i.e. ‘replacement’ organisms which colonise various sites when the patient is treated with antimicrobials. A knowledge of the normal flora present at various sites is important such that distinction may be made from ‘replacement’ organisms which have resulted from antibiotic therapy. The following are examples of normal flora:
- skin – coagulase negative staphylococci and diphtheroids;
- upper respiratory tract – ‘S. viridans’, diphtheroids, anaerobes, commensal neisseriae;
- lower gastrointestinal tract – coliforms, enterococci, pseudomonas, anaerobes (bacteroides, clostridia); and
- anterior urethra – skin flora (as above) or faecal flora (as above).
Commensal bacteria are potential pathogens, and infection may result if the balance is disturbed by a breach of the body defences or if an organism nor- mally a commensal at one site gains access to another site where it is not a commensal: e.g. E. coli, which is part of the normal flora of the colon, gaining access to the urinary tract and giving rise to a UTI. Broad spectrum antibiotics alter the normal flora, inhibiting sensitive organisms and allowing overgrowth of resist- ant bacteria which may result in serious infection. A detailed knowledge of the normal flora is required to distinguish normal flora in culture from pathogens responsible for infection.
Exogenous infection
Exogenous infection is derived either from other people or objects in the environment:
1. people: this may be from medical, nursing, or other patients either from infection, subclinical infection, or asymptomatic carriers;
2 inanimate objects (fomites): these include surgical instruments, anaesthetic equipment, ventilators, humidifiers, and parenteral fluids, particularly if drugs are added under non-sterile conditions; and
3. other sources: these include floors, blankets, urinary bottles, toilets, dust, air and air conditioning systems.
C.Diff
This is a recognized cross-infection problem. Control depends on a combination of hygiene measures such as isolation of patients with diarrhoea and hand wash- ing (alcohol does not kill spores) between contact with patients and careful use of problem antibiotics such as clindamycin and injectable cephalosporins.
Hepatitis B (i)
The hepatitis B virus is a double-stranded DNA virus. The incubation period is six weeks to six months and the period of infectivity is from six weeks before onset of the symptoms and possibly indefinitely thereafter. 10% of patients become chronic carriers. Antigen carriage is a risk for hospital staff, especially those in ‘high risk’ arreas, e.g. theatre staff. Dialysis units are often quoted as being a ‘high risk’ area but following outbreaks many years ago, all staff and patients are tested for HBsAg. Hepatitis vaccine is offered to all high risk healthcare workers. These categories involve surgeons, theatre nurses, pathology department staff, accident and emergency staff, staff in liver transplant units, workers in residential units for the mentally handicapped, staff of GI units and staff of infectious and communicable diseases units.
Hepatitis B (ii)
Hepatitis B may be transmitted by:
• blood transfusion;
• inoculation via sharps injuries from blood or blood products
• droplet transmission
• syringe and needle sharing in drug addicts;
• sexual intercourse with an infected partner;
• homosexual practices
• tattooing, ear piercing, etc. with unsterile
equipment.
A number of antigen-antibody systems occur relating to HBV. The three viral antigens are:
• HBsAg: hepatitis B surface antigen;
• HBcAg: hepatitis B core antigen; and
• HBeAg: hepatitis ‘e’ antigen.
Hepatitis B (iii)
Following infection, antibodies are formed against all three of the viral antigens but there are important clinical consequences of their identification. Infected persons and carriers have HBsAg and anti-HBcAg but lack anti-HBsAg in their blood. On recovery from infection, HBsAg disappears from the blood and anti- HBsAg becomes demonstrable together with anti- HBcAg. The e-antigen is found only in HBsAg positive sera and appears during the incubation period. The presence of HBeAg (e-antigen) implies high infectiv- ity. Carriers with a persistence of the e-antigen are much more likely to infect others. It has been shown that surgeons who possess the e-antigen may infect their patients during operative procedures.
Clinical presentations of hepatitis B include:
• acute hepatitis with clinical recovery
• acute fulminating hepatitis with death
• chronic active hepatitis with risk of developing cirrhosis and hepatocellular carcinoma.
Hepatitis C
Hepatitis C virus (HCV) is a single-stranded RNA virus. The incubation period is from six weeks to two months. About 0.7% of the population is chronically infected with HCV. Carriers are a source of infec- tion. HCV carriage is seen in drug addicts, recipients of blood and blood products before September 1991 (when testing was instituted), children of infected mothers and healthcare workers from occupational injuries.
Hepatitis B may be transmitted by:
• blood transfusion (before September 1991 in UK);
• syringe and needle sharing in drug addicts;
• mother to baby transmission;
• SHARPS injuries;
• sexual transmission occurs but is uncommon;
• tattooing, ear piercing etc. with unsterile
equipment; and
• sharing toothbrushes and razors.
HCV is identified by antibody testing. About 20% of people infected with HCV will clear the virus in the acute stage but will be antibody-positive. PCR will identify if active virus is still present.
The patient is often asymptomatic. Only about 25% become symptomatic and jaundiced. The severity of the symptoms does not necessarily equate with the extent of the liver disease.
Around 20% of those infected will clear the virus in the acute stage. Of those that do not, some will never develop liver damage. Many will develop only moderate liver damage with or without symptoms. Of the remain- der 20% will progress to cirrhosis within 20 years and of that 20%, some will progress to liver failure and some will develop hepatocellular carcinoma.
HIV (i)
HIV is a single-stranded RNA retrovirus. It produces DNA via the enzyme reverse transcriptase. DNA is incorporated into the host cells. HIV results in wide- spread immunological dysfunction. Infection results in a fall of the CD4 cell numbers and reduction of antigen-presenting cells. Immunological failure results in opportunistic infections and an increased risk of malignancy.
HIV may be transmitted by:
• sexual intercourse (heterosexual intercourse is likely to be the main cause in Africa and Asia; homosexual intercourse in the UK and North America);
• blood transfusion;
• intravenous drug abuse; and • mother to infant.
The following are at risk of becoming HIV positive:
• homosexual or bisexual males;
• prostitutes (male and female);
• intravenous drug abusers;
• haemophiliacs who were treated before routine
testing became available, i.e. October 1995; • sexual partners of the above; and
• children of infected mothers.
HIV (ii)
Asymptomatic viraemia occurs for up to three months after exposure and patients are infective during this period. ELISA test for HIV antibodies is negative at this stage. At seroconversion an acute illness can occur with fever, myalgia and joint pains. An asymptomatic phase then follows. Antiviral antibodies are now pre- sent in the blood and the patient is infective and this phase may continue for many years. Some patients may develop persistent generalized lymphadenopathy following seroconversion which lasts for up to three months with few or no constitutional symptoms. AIDS develops within 5–10 years.
However, an AIDS-related complex may occur before full-blown AIDS occurs. The AIDS-related complex is associated with CD4 cell count of 400/mm2. The virus infects lymphocytes, macrophages and monocytes, i.e. cells that are found in all body fluids. HIV binds the CD4 receptors on T helper lymphocytes (CD4 cells). After a long latent period, up to 8–10 years, the CD4 cell count begins to decline and hence the increase of immunosuppression with a risk of many opportunistic infections and also tumours. AIDS-related complex is characterised by fever lasting more than three months, weight loss, diar- rhoea, anaemia and night sweats. AIDS is diagnosed by the presence of an AIDS indicator disease (see below) with a positive HIV test.
Anti-HIV antibodies appear during the asymptom- atic phase after seroconversion. The CD4 count falls (400/mm2) in AIDS-related complex. The CD4 count thereafter falls further (200/mm2) when AIDS develops.
