Pathogens Transmitted from the Respiratory Tract | Microbiology

The following points highlight the top seven pathogens transmitted from the respiratory tract. The seven pathogens transmitted from the respiratory tract are: 1. Staphylococci 2. Pneumococci 3. Meningococci 4. Mycoplasma 5. Actinomycosis 6. Epidemic Parotitis  and 7. Psittacosis or Ornithosis.

Pathogen # 1. Staphylococci:

Skin and wound infections: Abscess: Osteomyelitis.

Staph, aureus. The most pathogenic staphylo­coccus has been described as the causative agent of suppurative process.

Morphology:

Staphylococci are spherical in shape, 0.8 -1 µ in diameter and form irregular clusters resembling bunches of grapes (Latin, staphyle, grapes). Staphylococci are Gram positive organisms; they are non-motile, form no spore, no capsule (Fig. 25.1).Cultivation:

Staphylococci are aerobes and grow well on nutrient agar media (Fig. 62.3) at 37°C and produce three types of pigments (lipochromes) : golden (Latin, aurum, gold); white (Latin, albus, white); lemon yellow (citreus). On the basis of pigment pro­duction they are classified into Staph, aureus, the most pathogenic; Staph, albus (less pathogenic); Staph, citreus (least pathogenic). They do not form spores, but they are somewhat resistant to drying; therefore they remain alive for several months under favour­able condition in dust or outside the body. They are found in upper respiratory tract.

Resistance:

Staphylococci are characterised by a relatively strong resistance to desiccation, freezing, sunlight and chemical substances. After desiccation, they can survive for more than six months. Repeated freezing and thawing do not kill the organisms. They survive for many hours under direct sunlight. They maintain their viability for more than one hour at 70°C.

At a temperature of 80°C, they are destroyed within 10 to 60 minutes and at boiling point, they instantly perish. A 5 per cent phenol solution kills the organ­ism in 15-30 minutes. Staphylococci are sensitive to aniline dye (brilliant green) which is used for the treat­ment of pyogenic skin diseases caused by this organ­ism.

Staphylococcal Toxins:

Pathogenic staphyloco­cci produce an exotoxin which is characterised by lethal, haemolytic and necrotic activity. Filtrates of sta­phylococcal broth cultures contain an enterotoxin which causes food poisoning on entry into the gastrointestinal tract. Leucocidin is a substance which destroys leucocytes.

This organism also coagulates blood plasma. The ability to coagulate plasma is a sta­ble property and is used for differentiating patho­genic from non-pathogenic strains. Coagulase is thermo resistant and can be isolated from staphylo­coccal cultures.

Staphylococci produce fibrinolysin which dis­solves blood clot; hyaluronidase which breaks down hyaluronic acid (cementing material between two body cells; lecithin’s destroys the lecithin; a sub­stance found in the protective membrane of human or sheep erythrocytes. Pathogenic strains isolated from humans produce alpha-haemolysin; those patho­genic to cattle produce beta-haemolysin.

Penicillinase or β –Lactamase:

As a result of ge­netic mutation, staphylococci acquire the power to produce penicillinase which destroys penicillin, i.e., it is resistant to penicillin.

Adaptive or induced enzyme:

Some-times, sta­phylococci produce penicillinase by their direct con­tact with penicillin, not by genetic mutation. Hence, the treatment with penicillin may induce the pro­duction of penicillinase. This enzyme produced in response to direct contact of staphylococci with peni­cillin is known as induced or adaptive enzyme.

Drug-fast Staphylococci and the nurse. Patient visitors, personnel may be carriers of Staph, aureus and become sources of the infection. If they carry drug-resistant staphylococci, they will become a dan­gerous source for the spread of the infection which cannot be controlled by antibiotics.

Therefore, the nurse is deeply concerned with this problem as she is in constant contact with patients suffering from in­fections caused by drug-fast staphylococci. If the causative organism is identified as drug-resistant strain, the further spread of these resistant strains should be prevented by washing hands, disposing of infected dressings, disinfecting bedding, dishes, ther­mo meter, bedpans, cleanliness of the rooms and wards, wearing gowns and masks. Only well trained, professional nurse can understand this problem and tackle by adopting all possible effective control meas­ures to check the spread of the infections.

Application to Nursing:

While handling staphylococcal infections, par­ticularly abscess, the nurse should take special care, so that the pus will not be discharged on anything as the pus is an explosive of drug-fast staphylococci and other pathogenic organisms.

Dressings of boils and other lesions should be discarded in a disinfectant jar or in a boiling water or tightly wrapped in several thickness of newspaper and fastened securely to pre­vent the escape of the infected dressings and burnt completely in an incinerator.

In the hospital, the nurse should pay much attention so that the pathogenic organisms are not disseminated from the bedding soiled with the nasal secretions into the environment and do not contaminate the fomites around the pa­tients.

Pathogenesis and diseases in man, Staphyloco­cci enter the body through the skin or mucous mem­brane where they overcome the lymphatic barriers and penetrate the blood; staphylococcal septicaemia sets in. Both exotoxins and the bacterial cells play an important role in the pathogenesis of diseases caused by staphylococci. So staphylococcal diseases can be considered as toxinfection.

Coagulase positive strains of Staphaureus produce six soluble toxins (A-F). Pathogenic staphylococci are responsible for a number of local lesions in man: abscesses, furuncles, periostitis, osteomyelitis, folliculitis, sycosis, dermati­tis, eczema, chronic pyoderma, peritonitis, meningi­tis, appendicitis and cholecystitis.

Predisposing factors for the formation of pyo­genic lesions of the skin and furunculosis are: diabe­tes mellitus, avitaminosis, excess perspiration, minor skin abrasions and skin irritation caused by chemical substances.

Staphylococcal sepsis and pneumonia in chil­dren are particularly severe diseases. Staphylococci play an essential part in mixed infections and are found together with streptococci in case of wound infec­tion, diphtheria, tuberculosis, actinomycosis. Pleurop­neumonia may lead to pulmonary abscess. It causes pharyngitis, tonsillitis, sinusitis.

Staphylococcal Food Poisoning:

Ingestion of food stuffs (cheese, curds, milk, cake, pastry, ice-cream etc.) contaminated with pre-formed toxin “enterotoxin B” liberated by pathogenic staphylococci in these foods may ensue food poisoning. (Enterotoxin refers to an exotoxin that affects the intestinal (enteric) tract (Greek, enteron = intestine).

The word enterotoxin should not be confused with endotoxin which means a toxin that remains inside the bacterial cell. (Greek, endon = inside of). The symptoms of food poisoning are nausea, vomiting, gastroenteritis (diarrhoea).Thorough cooking destroys the organism but not the en­terotoxin, so the enterotoxin is resistant to heat.

Prophylaxis of Food Poisoning:

1. Prompt refrigeration after cooking;

2. Discarding the stale or spoiled food.

Foods contaminated with staphylococci, i.e., any food that has been handled or exposed to peo­ple who are coughing, sneezing or talking may con­tain large amount of enterotoxin produced by sta­phylococci, if allowed to stand at kitchen tempera­ture for more than three to five hours. Staphylococcal food poisoning is rarely fatal.

Pathogen # 2. Pneumococci (Diplococcus Pneumoniae):

Pneumococci are primarily the causative agents of the infections of upper and lower respiratory tract, but are carried in the throat by many healthy persons. They are the commonest primary pathogens in lobar and bronchopneumonia and are frequently associated as secondary pathogens after primary virus infection of the respiratory tract. They are also associated with suppuration as empyema, meningitis, peritonitis and arthritis.

Morphology:

Pneumococci are lanceolate cocci occurring in pairs. They are Gram-positive, non-mo­tile and they have no spores. In the human body, they are encapsulated. The capsule can be demonstrated under microscope by India ink method or by capsular swelling reaction (Quelling reaction) by using spe­cific antiserum to capsular polysaccharide.

The cap­sule is responsible for:

(1) Smoothness of colony;

(2) Antigenic type specificity;

(3) Virulence.

Cultivation:

Pneumococci are aerobes, grow at 37°C, prefer 5 to 10 per cent CO₂ for primary culture. On a blood agar medium around the colony, there is a partial clearing of blood (alpha haemolysis) with greenish colouration like that of Strept. Viridans they are distinguished by being capsulated, bile soluble, sensitive to optochin, highly virulent and insulin fer­mentation.

Toxin Production:

Pneumococci do not produce exotoxin, but contain an endotoxin and liberate poorly a toxin which is characterised by its hemotoxic and fibrinolytic properties and by its ability to destroy leucocytes.

Serological Typing of Pneumococci:

Pneumo­cocci can be divided into 80 serologic types (Types, I, II, III etc.) on the basis of the type specific capsular polysaccharide Types I, II, III are virulent for human beings, while the rest possesses low virulence. The soluble specific substance or capsular polysaccharide is chemically different in each type.

Resistance:

Pneumococci live in dried sputum for two months. They are destroyed at 50-60°C within 10 minutes and in 3 per cent phenol within 1 -5 min­utes, are sensitive to optochin and bile salts.

Pathogenesis and Disease in Man:

Diplococcus pneumoniae causes lobar pneumonia (which derives its name from the fact that one or more entire lungs become infected).

Bronchopneumonia localizes in scattered patches throughout the lungs and may be caused by variety of organisms. Sometimes, streptococci or klebsiella pneumoniae may cause lobar pneumonia. The pneumococci may invade pleural cavity causing em­pyema, the meninges, causing meningitis, the peri­toneal cavity causing peritonitis. Because of the reduced body resistance (chilling, bronchitis, influ­enza, overstrain) the disease (lobar pneumonia) de­velops; use of antibiotics has considerably reduced death due to lobar pneumonia.

Transmission:

Saliva or sputum of patients with lobar pneumonia and as well as normal persons may contain D. pneumoniae.

The following are the main sources for the lobar pneumonia:

(a) The sputum and saliva of lobar pneumo­nia patients;

(b) Convalescent carriers; and

(c) Healthy carriers.

Another important vector is infected dust (drop­let nuclei). Since pneumococci are quite resistant to drying, they are found in the dust of the houses in which lobar pneumonia cases have occurred. The same mode of transmission is observed in strepto­coccal, staphylococcal infection, diphtheria, tubercu­losis.

Application to Nursing:

The nursing care procedure of the patient with lobar pneumonia has been modified because of the widespread use of sulphonamides and antibiotics, ul­timately the infectious stage of the disease has been considerably decreased. The nurse should be very much careful to disin­fect the dishes by boiling during infectious stage of the disease.

The linen should be boiled or adequately washed with hot water. Paper ‘wipes’ used for collec­tion of respiratory secretions and disposable hand­kerchiefs should be burnt. The patient with lowered body resistance should be isolated from other pa­tients to protect from the disease. In a ward, the nurse should develop barrier technique with adequate screening to protect other patients.

She should also follow precautionary measures to prevent the trans­fer of the infection. Since lobar pneumonia is frequently transmit­ted by droplet infection, the nurses and other medi­cal staffs should wear mask for their protection.

Pathogen # 3. Meningococci (Neisseria Meningitidis):

Meningococcus was isolated from cerebrospi­nal fluid (CSF) of the patient with meningitis.

Morphology:

Meningococcus is a coccus 0.6 – 1µ in diameter resembling a coffee bean and is found in pairs. The organism is Gram-negative. As distinct from pneumococci, meningococci are joined longi­tudinally by the concave edges while the external sides are convex. Spores, capsules and flagella are not formed. In pure culture, meningococci occur in tetrads (in fours) and in pus they are usually found within and less frequently outside the leucocytes.

Cultivation:

Meningococci are aerobes and do not grow on common media. They grow readily at pH 7.2 to 7.4 and at a temperature of 37°C in presence of 5-10 per cent CO₂ on chocolate agar medium and Thayer and Martin medium.

Fermentation Properties:

Meningococci cannot be differentiated from gonococci morphologically. They are distinguished by their ability to ferment mal­tose with acid production.

Oxidase Reaction:

Meningococci produce an enzyme oxidase which can be detected by adding fresh 1 per cent solution of an oxidase indicator, tetramethyl paraphenylene diamine. Over the sur­face growth of meningococci on the medium oxi­dase producing colonies turn purple in contact with this indicator.

Resistance:

Meningococcus is a microbe of low stability and is destroyed by drying in a few hours. By heating to a temperature of 60°C, it is killed in 10 minutes and at 80°C in one minute. This organism is very sensitive to a low temperature, hence the mate­rial containing meningococci should be transported in a Stuart’s transport medium which protects menin­gococci from adverse conditions. Meningococci are easily killed by chemicals containing silver and hence silver nitrate is used as drug externally in case of gono­coccal ophthalmia.

Antigenic Structure and Classification:

Menin­gococci were found to contain three fractions: Car­bohydrate (C) which is common to all meningococci; Protein (P) which is found in gonococci and in Type III pneumococci and a third fraction with which the specificity of meningococci is associated. Meningo­cocci are classified into group A, B, C and D on the basis of the chemical nature of the polysaccharide capsular substance. Recently, the number of types has increased to several, but only the first two are dominant.

Pathogenesis and Disease in Man:

Persons suf­fering from meningococcal infection and carriers are the sources of the infection. The infection is transmit­ted by the air droplet route. The causative agent is localised primarily in the nasopharynx. From here, it enters the lymphatic vessels, blood and causes the development of bacteriaemia. Thus, as a result of metastasis, meningococci pass into the meninges and produce acute pyogenic inflammation in the membranes (meninges) of the brain and spinal cord. The disease usually arises suddenly with high tempera­ture, vomiting, rigidity of the occipital muscles, se­vere headache and increased skin sensitivity. Later, paresis of cranial nerves develops due to increase in the intracranial pressure.

Dilatation of the pupils, dis­turbances of the accommodation and other symp­toms appear. A large number of leucocytes exist in cerebrospinal fluid (CSF) and the latter after punc­ture escapes with a spurt because of the high pres­sure. In some cases, meningococcal sepsis develops.

In such conditions, the organisms are found in the blood, joints and lungs. This disease mainly attacks children from 1 to 8 years of age. Before the discov­ery of antibiotics and sulphonamides, the death rate was very high (30-60 per cent). Drug resistance of this organism develops rapidly. Ceftriaxone (cefax-one) intramuscularly once a day is effective against purulent meningitis.

Transmission:

Meningitis can also be caused by other pathogenic microbes (streptococci, pneumo­cocci, staphylococci, tubercle bacilli and certain vi­ruses). These organisms, however, cause sporadic outbreaks of the disease, while meningococci may cause epidemic meningitis. The population density plays an important role in the spread of meningitis. During epidemic out­breaks, there is a large number of carriers for every individual affected by the disease.

Diagnosis:

Meningococci can be demonstrated in smear from centrifuged CSF obtained by the lum­bar puncture. This is of great importance for immedi­ate diagnosis and therapy.

Application to Nursing:

In dealing with epidemic meningitis, the nurse should follow the same precautions adopted for in­fections transmitted by the oral and nasal secretions (lobar pneumonia and scarlet fever).

Pathogen # 4. Mycoplasma:

Mycoplasma is the smallest prokaryotic organ­ism to grow in cell free culture medium. Out of 8 or 9 species, Mycoplasma pneumoniae is the only patho­gen. Clinically M. pneumoniae infections take the form of a febrile bronchitis or pneumonia with generalized symptoms — malaise (which may over­shadow the respiratory symptoms), myalgia, sore throat headache, cough, which starts around the third day, is characteristically troublesome.

Coryza is unu­sual, but nausea and vomiting may be a feature. It is also an important cause of otitis. Complications are — rashes, urticaria, maculopapular rash, erythema multiform (vesicular and bulbous lesions on muco­cutaneous junctions), meningitis, encephalitis, some­times haemolytic anaemia. In 5 to 15 years age groups and in both sexes, M. pneumoniae may be the major cause of (20-40%) of all non-bacterial pneumonia.

Treatment:

Tetracycline is the drug of choice. The spread of the disease can be prevented by proper disinfection and disposal of sputum.

Pathogen # 5. Actinomycosis:

Actinomycosis occurs as a chronic granuloma­tous infection in men and animals. In man, the infect­ing species is Actinomycosis israelii which occurs commensally in the buccal cavity.

Morphology:

Actinomyces are intermediate between bacteria and fungi. They have non-septate mycelium with aerial sporangia. They grow as colo­nies in the tissues, called as” sulphur granules” which are macroscopic. If these granules are crushed be­tween the two slides, stained by Gram method and examined under microscope, the central filamentous mass is Gram-positive and the surrounding zone of radiating clubs is Gram-negative.

These clubs repre­sent lipoid material derived from the host tissues to prevent further invasion by filamentous growth. When such smear preparations are stained by Ziehl-Neelsen, by replacing 20 per cent sulphuric acid by 1 percent for decolourisation, the peripheral clubs are stained acid-fast and the central mycelial mass is non-acid-fast. Club formation is less frequent in hu­man than in animal lesions.

Resistance:

Actinomyces are very resistant, with­stand a temperature of 60°C for 1 hour and remain viable for a longer period when dried; their spores are particularly resistant.

Clinical Infection:

Actinomycosis may result from endogenous infection when actinomyces pen­etrates from the digestive tract. The chewing of the grain, skin and mucosa injuries and particularly cari­ous or worn out teeth facilitate the infection. The causative agents spread gradually in the connective tissue and between the muscles and are circulated in the blood or lymph.

The infectious process is accom­panied by the formation of suppurative foci and fistulae which open within or outside the body. The dis­ease is characterised by chronic inflammation with subsequent development of suppurative process. Hard infiltrates or granulomas form at the site of localisa­tion of the organism.

The skin becomes purple blue and the infiltrates so often, necrotise and discharge pus which has an offensive odour and contains sulphur granules made of threads of actinomyces. Affection with pathogenic actinomyces is mostly accompanied by secondary pyogenic infection.

According to clinical manifestations, actinomy­cosis of the face and neck, pulmonary actinomycosis, abdominal actinomycosis, actinomycosis of internal organs, skin actinomycosis, skin and muscular actino­mycosis, bone and muscular actinomycosis, actino­mycosis of the nose, ears, larynx, pharynx, eyes, cen­tral nervous system etc. can be differentiated. The involvement of lungs is followed by pleuropneumo­nia or kidney metastases, skin abscess.

Laboratory Diagnosis:

The sulphur granules in the pus can be harvested by shaking the pus with water in a test tube; after standing for few minutes, the granule sediments may be collected with a cap­illary pipette. A granule would be crushed between two slides, fixed and stained by Gram stain method and by modified Ziehl-Neelsen technique.

Treatment:

Before the advent of penicillin, the surgical treatment was adapted. Penicillin is the drug of choice. Other antibiotics were also prescribed in combination with iodine, X-ray therapy and surgery. Human actinomycosis includes Madura disease (Madura Foot or maduromycosis) which is caused by Nocardia madurae and other actinomyces. It is a chronic foot infection, the foot becoming swollen and deformed. At times, the process may be local­ised in the shank, hands, abdomen etc.

Following penetration of the organisms, nodules are produced at the site of entry, the skin becomes red violet or brown, the nodules soften and break through the skin forming fistulae which discharge pus. Patients are treated with penicillin in combination with sulphonamides. Chlortetracycline and oxytetracycline are also used.

Respiratory Fungus Disease:

Histoplasmosis and coccidioidomycosis are im­portant and widespread infections of respiratory tract caused by fungi. They are not transmitted from per­son to person, but mainly from soil.

Pathogen # 6. Epidemic Parotitis (Mumps) Virus:

Mumps is an acute contagious disease charac­terised by a large painful swelling of one or both pa­rotid glands. Mumps is known from ancient time and was one of the first infections described by Hippocrates. The name is derived from the numbing speech which is result of the pain on moving the jaw. Usually, there is a constitutional reaction and other glands (testes, pancreas, parotids) are involved.

Pathogenesis and Disease in Man:

The parotitis virus causes fever and inflammation of the parotid, sublingual and submandibular glands. The disease is prevalent amongst children. Mumps is a very conta­gious disease. Severe cases are accompanied by viremia. In addition to parotitis, the virus penetrates other organs and produces orchitis and meningitis. Com­plications are polyneuritis, paresis of facial and au­ricular nerves, and impairment of hearing and visual dis­turbance.

Immunity:

It is life long immunity after the dis­ease is produced.

Treatment:

Drugs (corticosteroids and gamma globulins) are prescribed for symptomatic treatment. These drugs reduce the severity of the disease but do not prevent the development of meningitis and orchitis.

Prophylaxis:

Isolation of patients until they re­cover. Patients are discharged from the hospitals only when all clinical manifestations of the disease have disappeared. The disinfection is not required. Specific prophylaxis is by injection of gamma globulins and a vaccination with a live vaccine prepared from a strain of Mumps virus which has lost its pathogenicity as a result of passage on chick embryo. It is inoculated intracutaneously in a single dose.

Rhinovirus:

The viral nature of contagious rhinitis (common cold) was known more than 50 years ago. Rhinovirus can be cultivated in human kidney culture. It is iden­tical with enterovirus in size, resistance to ether and in the non-pathogenicity for suckling mice.

Pathogen # 7. Psittacosis or Ornithosis:

Previously called Psittacosis — Lymphogranu­loma venereum —Trachoma group (PLT organisms) or the TRIC group (Trachoma—Inclusion Conjuncti­vitis organisms) are included in the family chlamydiae.

Morphology:

These organisms are small, non- motile, Gram negative, obligate, intracellular parasites which have two forms of cells: Small and large forms.

Cultivation:

They can be cultivated in chick em­bryo or in mice and tumour cells.

Psittacosis (Gr. Psittakes, Psittacine) or Ornitho­sis (Gr. ornis, bird) is acquired by inhalation of infected aerosols or dust from birds during handling chickens, pigeons, geese, turkeys etc., while killing, plucking or cleaning for the table.

The incubation period is ten days and the illness ranges from influenza-like syn­drome with general malaise, fever, anorexia, rigor, sore throat, headache, photophobia to a severe illness with delirium and pneumonia with consolidation similar to bronchopneumonia and the sputum is scanty. Pneu­monia foci are accompanied by dyspnoea, cough and pain in the chest and characteristic of Ornithosis. X- ray reveals lobar pneumonia.

In short, the clinical picture of Ornithosis is simi­lar to that of atypical pneumonia, influenza, typhoid fever, typhus fever, lobar and catarrhal pneumonia and Q fever. Infection from person to person by air droplet route is also possible.

Resistance is very high. They survive for longer period in desiccation state and at low temperature. At-70°C, they remain viable for two years. They are killed by heating at 60°C – 70°C in 10-15 minutes. They are sensitive to common disinfectants. Immunity is of short duration and the reinfec­tion is possible.

Treatment:

Chortetracycline, oxytetracycline and streptomycin are effective.

Application to Nursing:

Just after early diagnosis by the physician, the patient should be sent to isolation ward and hospitalization. Nurses should wear masks and regularly wash hands with 0.5 per cent chloramine solution; patients should be discharged only after complete recovery.

Premises and patients’ clothing’s should be disinfected. The patients’ sputum should be disinfected with 4 per cent chloramine solution; 5 per cent cal­cium chloride; 0.5 per cent potassium hydroxide or sodium hydroxide and 5 per cent solution of Lysol.