Infection Control


6
Infection Control


Jane Devaney


Philip Leverhulme Equine Hospital, University of Liverpool, Wirral, United Kingdom


6.1 Disease Transmission


To understand how infectious diseases are established and spread, the following definitions must be taken into account:



  • Infection is the colonisation of an individual host by a foreign microorganism. Infectious agents that cause harm are called pathogens.
  • Disease occurs when normal body processes are sufficiently impaired that a reduction in performance occurs. This leads to the development of clinical signs.
  • A contagious disease is a communicable disease that can be spread rapidly from horse to horse through direct contact (touching another horse who has the infection), indirect contact, (touching a contaminated object), or droplet contact (inhaling droplets produced by an infected horse when they cough or sneeze).
  • Nosocomial infections are also known as hospital‐acquired infections. These are a subset of diseases that are acquired in a healthcare setting, such as a veterinary hospital.
  • Carriers are infected animals which continue to shed infective agents despite showing minimal or no signs of the disease [1].
  • A zoonotic disease is a disease that is transferable from animals to humans.
  • The incubation period is the time lag between the exposure to a pathogenic organism and the onset of symptoms.
  • A notifiable disease is a disease that must be reported to the Animal and Plant Health Agency (APHA). Failure to do so is an offence. Table 6.1 displays a selection of equine notifiable diseases.

Transmission


In order for pathogens to succeed and spread, they need to successfully infect a host. Pathogens spread between hosts via a number of different methods [1]:



  • Direct transmission: This involves the spread of pathogens by direct contact. For example, equine influenza is spread via aerosol droplets, which are coughed out by infected horses and inhaled by non‐infected horses.
  • Indirect transmission: This occurs if an infection is acquired from a contaminated environment or via a vector.
  • Mechanical vectors: Also known as fomites. These may be inanimate objects such as bedding, grooming equipment, feed buckets and haynets.
  • Biological vectors: These are organisms that may convey infectious agents from one host to another, but do not cause disease themselves. For example, WNV is spread by mosquitoes, and so they are considered to be biological vectors.
  • Horizontal transmission: Refers to the direct or indirect spread of infection between members of the same generation.
  • Vertical transmission: Refers to the spread of infection from the dam to offspring. An example of this is the spread of EVA from a mare to her unborn foal.

Routes of Transmission


Different infective agents may be excreted by a variety of routes, including:



  • Saliva: Rabies
  • Blood: Equine infectious anaemia (EIA)

    Table 6.1 Equine notifiable diseases.


    Source: Jane Devaney and Marie Rippingale.












































































    Disease name Causal agent Clinical signs Method of transmission Prevention and control
    Rabies
    (Zoonotic)    		 Virus Affects all mammals. Behaviour changes: friendly animals may become cautious, shy animals may become bold. Hypersensitivity to noise or light. Increased aggression. Eyes taking on a staring expression. Drooping lower jaw and hypersalivation. Itching and increased thirst. In the final stages of rabies, clinical signs include weak muscles, dysphagia, drooping eyelids and saliva frothing at the mouth. General paralysis followed by convulsions and coma preceding death. Some animals will show no signs at all, so laboratory tests are required to confirm the diagnosis [2]. Infection is through bite/saliva from an infected animal [2]. Treatment not available for animals. Euthanasia is recommended [2].
    Vesicular Stomatitis
    (Zoonotic)    		 Virus Pyrexia, blisters on mouth and tongue. Lameness and hypersalivation [3]. Spread by flies and direct contact Strict biosecurity and isolation of affected animals.
    Equine Infectious Anaemia (EIA) Virus Some infected animals do not show signs. Clinical signs can include recurring pyrexia, lethargy, weakness and depression, loss of appetite and weight loss. Incubation period 1–3 weeks but can be up to 3 months [4]. Infection can be spread by large horse flies. It can also be spread by the venereal route and via vertical transmission. The virus can also be spread by iatrogenic transfer of blood, either in blood transfusions or on contaminated needles, surgical instruments and dental equipment [4]. There is currently no effective treatment for EIA and no vaccine available. All infected horses, including those that show mild or unapparent signs, become carriers and are considered potentially infectious for life. Infected animals must either be destroyed or remain permanently isolated from other equids to prevent transmission. A request to exempt an infected equine(s) from destruction will be considered taking into account the local situation and the need to preserve genetic diversity, or other characteristics, and the need to prevent exposure of other susceptible animals from potential infection both at the time and in future. Requests are considered on a case‐by‐case basis [4].
    Equine Viral Arteritis (EVA) Virus Clinical signs include abortion, conjunctivitis, watery eyes, swelling of testicles or udder, also around the eyes and lower legs, pyrexia, depression, anorexia, lethargy and stiff movement. Some infected horses will show no clinical signs. In rare cases, the disease can cause severe clinical signs and even death in young foals [5]. Spread via inhalation of respiratory particles. Can also be spread via the venereal route by either natural covering or artificial insemination (AI) and on fomites. Stallions can carry the disease for extended periods without showing clinical signs. Mares can spread the disease through vertical transmission to the foal or via the venereal route to a stallion [5]. Good biosecurity measures. Isolation of new horses, and testing all stallions, teasers and mares before breeding. Vaccination of breeding stallions should be considered. If EVA is confirmed in a stallion, it will remain under breeding restrictions until the risk is mitigated. This can be done through castration, export or repeated tests showing that it no longer has the virus. Until the risk has been mitigated, the stallion cannot be used for breeding except under licence from APHA. To mitigate the risk of disease spreading, the infected stallion may be named and its location publicised [5].
    West Nile Virus (WNV) Virus Ataxia, pyrexia, listless/dullness, drooping lips, collapse, and inability to rise. Can lead to blindness, and seizure activity [6]. Spread by mosquitoes Incubation 3–15 days [6]. Vaccination can prevent encephalitis; supportive treatment can be given with varied success [6].
    African Horse Sickness (AHS) Virus Respiratory form:
    Frothing and discharge from nostrils.
    Fever, slow, heavy breathing, coughing. Swollen face. Sudden death. Death rate 90%
    Incubation period 3–5 days
    Cardiac form:
    Swelling and redness around the eyes. Swelling of the head. Inability to swallow. Possible colic symptoms. Petechial haemorrhages on mucous membranes. Slow onset of death. Death rate 60%
    Mixed form:
    Mild respiratory signs. Swelling of head and eyes. Incubation period 2–14 days [7].    		 Spread by midges, no direct spread between horses. If an outbreak were to occur the premises would be isolated and the affected animals destroyed, all other horses would be isolated. There is no vaccine for any serotype of AHS currently available in the United Kingdom or parts of Europe though research into safe and effective vaccines is on‐going. Vaccines available in Africa are not suitable for use in the United Kingdom. A vaccine bank is being developed but will only be used in a strictly controlled manner, in an emergency situation [7].
    Anthrax
    (Zoonotic)    		 Bacterial infection caused by Bacillus anthracis Hot painful swellings of the throat and colic. Inhaled, ingested, or contact with skin lesions. Spores can survive for decades or even centuries. Spores are found on infected animal carcasses, wool, hair and hides [8]. Strict isolation and biosecurity protocols.
    Glanders and Farcy
    (Zoonotic)    		 Bacterial infection caused by Burkholderia mallei Coughing, nasal discharge, and fever. Ulcerated nodules on the skin or internal organs. Nodules on the nostrils, lungs and other internal organs are known as Glanders, those involving the limbs or body are known as Farcy. Chronic infection can last for years and result in death from chronic lung damage. Acute infections lead to death within days [9]. Infection is spread through contaminated food, water, or equipment. Animal to human infection is possible although rare and only possible when handling a case with obvious disease [9]. Isolation of infected animals and strict biosecurity measures including wearing masks, goggles, and gloves. Antibiotic treatment may be considered. Infected horses become carriers and must be isolated for life [9].
    Contagious Equine Metritis (CEM) Bacterial infection caused by Taylorella equigenitalis CEM is a venereal disease. Stallions do not show clinical signs of the disease, but they can carry it. Mares will exhibit discharge from swollen genitals, especially 1–6 days after mating, lesions or damage to the skin, weakness/stiffness/lack of co‐ordination and an inability to move [10]. Spread via the venereal route. Pre‐breeding swabs should be taken from the mare, the stallion should also be tested. Laboratories are legally required to report infection to APHA. Infected animals should be treated and retested as clear before breeding. Strict biosecurity controls should be adhered to. Treatment includes washing the affected area, and treatment with topical antibiotics.
    Epizootic Lymphangitis Fungal infection caused by Histoplasma farciminosum Patches of damaged skin can appear anywhere on the body. Swollen and hard glands. Thick yellow scabs can form over patches of ulcers. Nasal discharge or ulcers in the nostrils. The likelihood of fatality increases with time, therefore earlier treatment is more effective. More commonly seen in equids younger than six years of age [11]. Infection is through wounds and equipment such as riding equipment that may contact open skin. It is also spread by flies. Can live in soil for up to 15 days [11]. Strict biosecurity on the premises, quarantine and euthanasia of infected animals.
    Dourine Parasitic infection of Trypanosoma equiperdum Fever. Swelling of genital areas or udders and the surrounding skin. Fluid discharge from genitals (in mares). Lesions or damage to the skin. Stiffness and weakness. Lack of coordination. Inability to move. Dourine is often fatal, although some animals show no signs and recover from the disease [12]. Spread via the venereal route. No treatment available, euthanasia recommended in affected animals.

  • Urine: Leptospirosis
  • Faeces: Salmonella
  • Milk: Strongyloides westeri
  • Across the placenta: Equine viral arteritis (EVA)
  • By aerosol: Equine influenza
  • By skin contact: Dermatophytosis (ringworm)
  • During sexual contact: Dourine
  • Via fomites: Streptococcus equi

6.2 Microorganisms


It is beyond the scope of this chapter to discuss all microorganisms that cause disease. Therefore, only the main disease‐producing microorganisms that affect equine patients will be discussed. Microorganisms vary in size and structure. The major similarities and differences are shown in Table 6.2.


Table 6.2 Major similarities and differences between different types of microorganisms.


Source: Table reproduced with kind permission from BSAVA Textbook of Veterinary Nursing 5th Edition © BSAVA.





















































Characteristic Bacteria Viruses Fungi Protozoa Algae
Size 0.5–5 μm 20–300 nm 3–8 μm (yeasts) 10–200 μm Approximately 20 μm
Cell arrangement Unicellular Non‐cellular Unicellular or multicellular Unicellular Unicellular or multicellular
Cell wall Present; mainly peptidoglycan Absent Present; mainly chitin Absent Present; mainly cellulose
Nucleus No true membrane‐bound nucleus Absent Membrane‐bound nucleus Membrane‐bound nucleus Membrane‐bound nucleus
Nucleic acids Deoxyribonucleic acid (DNA) and Ribonucleic acid (RNA) DNA or RNA but never both DNA and RNA DNA and RNA DNA and RNA
Reproduction Asexual by binary fission Replicate only within another living cell Asexual and sexual by spores, budding in yeast Asexual and sexual Asexual and sexual

4.2 Viruses


Shape and Structure


Viruses are much smaller than bacteria and consist of a single‐ or double‐stranded nucleic acid (deoxyribonucleic acid (DNA) or ribonucleic acid (RNA) but never both) forming a central core, surrounded by a protein shell called a capsid. Together, these two parts form a nucleocapsid [13]. The different shapes of nucleocapsid are as follows:



  • Helical
  • Icosahedral
  • Complex (poxvirus)
  • Composite (some bacteriophages) [13]

Each helical or icosahedral shape of the nucleocapsid can be enveloped or non‐enveloped (see Figure 6.1). This gives four basic shapes for viruses. There are no animal viruses that are helical and non‐enveloped, so viruses affecting equine patients can be grouped into the other three types [13].

Four schematic diagrams of Helical and icosahedral viruses are titled as follows. 1. helical naked. 2. Helical enveloped. 3. Icosahedral naked. 4. Icosahedral enveloped.

Figure 6.1 Helical and icosahedral viruses may be enveloped or non‐enveloped (naked).


Source: Figure reproduced with kind permission from BSAVA Textbook of Veterinary Nursing 5th Edition © BSAVA.


Reproduction


Viruses are incapable of reproduction without a host cell and can only attach to cells that carry a compatible receptor. For example, influenza viruses can only attach to ciliated epithelial cells in the respiratory tract [13]. This specificity is known as tissue tropism. Viruses can only target a small number of host species, for example, the equine herpes virus cannot infect dogs.


Virus replication can take place via either the lytic or lysogenic cycles. These cycles differ in their mechanisms and outcomes.


Lytic Cycle:



  • Attachment: The virus attaches to the host cell surface.
  • Entry: The virus injects genetic material (DNA or RNA) into the host cell.
  • Replication and Transcription: The viral genome takes over the host cell’s machinery to produce viral components, including more viral genetic material and viral proteins.
  • Assembly: New viral particles are assembled inside the host cell.
  • Release: The host cell is often lysed (broken open), releasing newly formed viral particles, which can then infect neighbouring cells to repeat the cycle.
  • In the lytic cycle, the virus immediately begins to replicate upon entering the host cell, leading to the rapid production of new viral particles and ultimately causing the destruction (lysis) of the host cell.

Lysogenic Cycle:



  • Attachment and Entry: Similar to the lytic cycle, the virus attaches to the host cell and injects its genetic material.
  • Integration: Instead of immediately hijacking the host cell’s machinery, the viral DNA integrates into the host cell’s genome, becoming a part of it. This integrated viral DNA is called a prophage.
  • Replication: As the host cell replicates its own DNA, it also replicates the integrated viral DNA (prophage) along with it.
  • Induction: Under certain conditions (such as environmental stress), the prophage may become active again.
  • Entry into Lytic Cycle: The prophage excises itself from the host genome and enters the lytic cycle, leading to the production of new viral particles and lysis of the host cell, similar to the steps in the lytic cycle.
  • The lysogenic cycle involves a period of dormancy where the virus’s genetic material becomes part of the host cell’s genome without immediately causing harm. However, the virus can later re‐enter the lytic cycle to produce more viral particles.

The key difference between the lytic and lysogenic cycles lies in their outcomes and the timing of viral replication. The lytic cycle involves immediate viral replication and destruction of the host cell, while the lysogenic cycle involves integration of the viral genome into the host cell’s genome, followed by a period of dormancy before reactivation and subsequent lysis of the host cell.


Viral Diseases Affecting Equids


Equine Herpes Virus (EHV)

Strains 1–9 exist, with EHV‐1, ‐3 and ‐4 known to cause the most serious health risks. EHV‐1 causes four main health issues, including neurological disease, abortion in mares, neonatal death and respiratory disease. EHV‐4 causes respiratory disease and occasional abortion in mares. Both EHV‐1 and EHV‐4 are spread directly via aerosol droplets in the air from coughing horses and indirectly via people, tack, feed and equipment. In the case of EHV‐1, contact with aborted foetuses and placentae associated with abortions can spread the disease. The incubation period is from 24 hours to 14 days, typically around 4–6 days. Clinical signs of respiratory disease are fever, nasal discharge, dry cough, loss of appetite and lethargy. Neurological signs are incoordination of the limbs (mainly hind), ataxia, loss of bladder tone and recumbency. Isolation of all new arrivals on a yard for 21 days is essential. Treatment includes good nursing care, anti‐inflammatories and, in some cases, intravenous (IV) fluids. Antibiotics will not treat the virus, but may be prescribed if a secondary infection occurs. A vaccine is available for EHV‐1 and ‐4 (see Chapter 5), but it is seldom effective against neurological forms of the disease.


Equine Rhinitis Virus (ERV)

ERV should not be confused with rhinopneumonitis, which is caused by EHV. There are two forms of ERV: equine rhinitis A (ERA) and equine rhinitis B (ERB). Serologic studies show that ERV is distributed worldwide. Spread is by aerosol droplets as the horse sneezes, coughs, or snorts and by fomites such as grooming and feeding equipment. ERV causes mild to severe respiratory disease, which can affect the upper and lower airways. A vaccine is available in the United States. New horses should be quarantined. Treatment is the same as for EHV.


Information on equine influenza can be found in Chapter 13. See Table 6.1 for information regarding EIA, EVA, WNV and rabies. These are notifiable, viral diseases.


Bacteria


Shape and Structure


All bacteria are named according to the binomial system [13]. The first word starts with a capital letter and indicates the genus (plural: genera) to which they belong e.g. Escherichia. This is followed by the species name all written in lower case e.g. coli. Therefore, Escherichia coli is one of the species of the genus Escherichia, just as Homo sapiens (modern humans) is one of the species of the genus Homo [13]. The generic name is frequently shortened to initial letter, for example, Escherichia coli becomes E. coli; Staphylococcus aureus may be seen written as Staph. aureus. Both generic and specific names should be written in italics. The genus name can also be used with the abbreviation sp. (for one species) or spp. (denoting multiple species of the same genus) e.g. Staphylococcus spp. [13]. Many species of bacteria have characteristic arrangements that are useful in identification (Figure 6.2).


Bacteria can be classified according to their shape. The different shapes of bacteria include:



  • Bacilli (or bacillus for a single cell) are cylindrical or rod‐shaped cells. Some bacilli are curved, and these are known as vibrios [13].
  • Cocci (or coccus for a single cell) are spherical cells, sometimes slightly flattened when they are adjacent to one another.

    • Pairs of cocci are called diplococci.
    • Rows or chains of such cells are called streptococci.
    • Grape‐like clusters of cells are called staphylococci.
    • Packets of eight or more cells are called sarcinae.
    • Groups of four cells in a square arrangement are called tetrads.

  • Spirilla (or spirillum for a single cell) are curved bacteria which can range from a gently curved shape to a corkscrew‐like spiral. Many spirilla are rigid and capable of movement. A special group of spirilla known as spirochaetes are long, slender and flexible.

The structure of a generalised bacterial cell is depicted in Figure 6.3. Some of the structures depicted in Figure 6.3 are common to all bacterial cells; however, some are only present in certain species or under certain environmental conditions [13]. Bacteria are generally encased in a cell wall, which can vary in thickness and composition [14]. A capsule usually sits on the outside of the cell wall for protection purposes. Within the cell wall sits the cell membrane, which surrounds the cytoplasm. The bacterial chromosome contains the genetic material of the cell, and this is housed within the cytoplasm. Each cell may have one or more plasmids, which play an important role in antimicrobial resistance. Some bacteria possess other structures outside the cell as follows:

Six schematic diagrams in a row are titled as follows. 1. Bacilli. 2. Vibrios. 3. Diplococci. 4. Streptococci. 5. Staphylococci. 6. Spirochaete.

Figure 6.2 Different shapes of bacteria.


Source: Rosina Lillywhite.



  • Flagella: These help with the movement of the cell
  • Pili: These are involved in cell reproduction
  • Fimbriae: These are involved in the adherence of the bacteria to host cells [14]

The key differences in cell wall structure between gram‐positive and gram negative bacteria result in their differential staining patterns:


Gram Positive Bacteria:



  • These bacteria have a thick layer of peptidoglycan in their cell wall, which retains the crystal violet‐iodine complex during the decolourisation step.
  • They lack an outer membrane.
  • After staining, gram positive bacteria appear purple or blue under the microscope.

Gram Negative Bacteria:



  • These bacteria have a thinner layer of peptidoglycan in their cell wall, which does not retain the crystal violet‐iodine complex well during decolourisation.
  • They possess an outer membrane composed of lipopolysaccharides (LPS) that act as a permeability barrier.
  • During the decolourisation step, the outer membrane is disrupted, allowing the crystal violet‐iodine complex to be washed away more easily.
  • After staining with the counterstain, gram‐negative bacteria appear pink or red under the microscope [14].
A schematic diagram of the bacterial cell includes the following. Mesosomes, cell membrane, cytoplasm, storage granules, cell wall, capsules and slime layers, flagellum, and bacterial chromosome. The explanation is also included in blocks.

Figure 6.3 Components of a generalised bacterial cell and their functions.


Source: Samantha Elmhurst and Rosina Lillywhite.


Growth


Bacteria can only grow and reproduce when environmental conditions are suitable [1]. Requirements for this are as follows:

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Mar 1, 2026 | Posted by in NURSING & ANIMAL CARE | Comments Off on Infection Control

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