Rinderpest

Cattle plague
Description:
A disease of cloven hoofed animals which is also considered as the most lethal plague
in cattle characterized by fever, necrotic stomatitis, gastroenteritis, lymphoid necrosis and high
mortality.

2nd virus eradicated (measles 1st virus eradicated)

Etiology:
Morbillivirus, paramyxoviridae (canine distemper)

 Replication in the epithelial and lymphoid tissues

 GIP and Respiratory tracts

Transmission & Epidemiology:

Clinical Findings

Lesions and Diagnosis

Lymphadenopathy
Remnants of the virus (Intracytoplasmic / intranuclear inclusion bodies
PCR for serology then followed by RTPCR for seropositive animals

Greyish epithelium
Control
 Peste des petits of ruminants (PPR)

Very much the same with rinderpest but PPR only infects small ruminants.
Cross immunity when suppressing rinderpest also suppress PPR. But when the rinderpest is
eradicated. PPR doesn’t have a break anymore due to eradication of rinderpest. This causes
the rapid spread.
Clinical findings and lesion

IP is way shorter compared to rinderpest

Putrid odor due to necrosis of the epithelium
Looks like abomasitis / hemocosis in small ruminant
Slough of peyer’s a patches is due to lymphoid involvement
Diagnosis

Control
 Foot and mouth disease, Aphthous fever
Description: A highly communicable disease of cloven-hoofed animals characterized by fever
and vesicles in the muzzle, teats, and feet of affected animals.
Somewhat the same appearance with rinderpest in a way it is able to create lesion on
the epithelium. However, the very difference is that this start at vesicular growth as compared to
rinderpest that right away creates necrotic foci
Historical features:

 2006 – start of FMD eradication campaign

 2011 – Eradicated in the country (as declared by OIE)
 Philippines declared as FMD-free without vaccination
2015/2016 ~ 5yrs after: FMD free without vaccination
Transmission & Epidemiology:

 All species of Order Artiodactyla (same susceptibility with rinderpest)

 Inhalation of ingestion (from infected source to susceptible animals)
 Direct contact with infected animals
 Contaminated animal products (Very hardy virus, can survive in the environment of the
animal host)
 Airborne virus (200 km/miles within the air) inside droplets
 Mechanical transmission of virus on people, vehicles, etc.
 Shed in the milk
Etiology
Apthovirus, Picornaviridae (very small viruses)
 Serotypes: (based on the antibody response of the animal)
o A, O, C (present in the Philippines)
o Asia 1, SAT 1, 2, 3 (present only in Africa)
 Viability:
o 14 days -dry fecal matter
o 39 days – urine
o 28 days – soil surface in fall
o 3 days – soil surface in summer
o ~24h – in human (never ever go to other farms when there is a disease outbreak
 Environment stability
o pH 6-9
o >56°C
o Resistant to lipid solvents (ether, chloroform)
o Ionic Disinfectants (NaOH, NaHCa, acetic acid)
Pathogenesis
Direct and indirect contact, mechanical vectors, Air (Labay sa sapa)

IP: 3-8 days small ruminants / 2-14 days large ruminants (same with other dis)

1. Oropharynx = initial site of replication

Blood/lymphatics

2. Epithelium of the mouth, muzzle, feet and teats

(Areas often suspected to mechanical trauma)

Vesicles grow and erupt at 48 hrs.

Secondary bacterial infection / heals

50% of recovered ruminants becomes carrier
(Pharyngeal mucosa)

 3.5 yr. = cattle

 9mo. = sheep
 >5 yrs. = buffalo
Clinical Findings & Lesions

 Initial sign is pyrexia (up to 41.1°C 1-2 days before other clinical signs)
 Non-specific signs:
o Fever
o Dull, depressed, anorexia, loss of condition
o Reduction in milk yield
 Nasal discharge (serous to mucopurulent) usual pattern for many viral causes of rhinitis
 Vesicles:
o Mouth (+/- salivation)
 Gingiva, gums, tongue
 Buccal cavity and nares
o Feet (+/- lameness)
o Mammary glands
o Death in young animals (abortion, myocarditis almost always apparent if there is
bacterial infection / Virial Infection /any septicemic condition for your aborted
fetus and even in the young units)

Most like to find salivation, erosion, and vesicular growth.

Diagnosis

 Fresh vesicular fluid and epithelial tissues /scrape epithelial tissue

 1-gram refrigerated samples
 Phosphate-buffered saline (or equal parts of PBS and glycerol)
PCR

 Oropharyngeal fluid
 Through probang cup pr pharyngeal swab
ELISA

 Surveillance in countries with endemic status (Not used for confirmatory)

 If seropositive is present we can proceed to PCR/Virus Neutralization Test
Virus Neutralization Test (VNT)

 Used in the Philippines to test pigs before importation

Baby Hamster Kidney (BHK)

 Preferred culture medium (For virus isolation)

Virus isolation

 Primary Bovine Thyroid Cell Culture

Treatment, Control, and Prevention

 No specific treatment
 Supportive (Flunixin meglumine) Search dose
  Quarantine
 Movement control
 Vaccination
o Killed trivalent (A, O, C)
o Endemic areas
o 3x a year

Peste des petits still occurs in India and Middle East and still spreading to the east. There is a
fear nowadays that Peste des petits could reach south east Asia. SEA has a lot of population of
small animal

Principles for controlling a FMD outbreak:

“Prevent transmission from infected to susceptible animals”
 Production of virus
o Cull infected and in-contact animals, +- dangerous contacts if high-risk
 Potential for direct contact between animals
o Movement restrictions
 Virus survival time in the environment
o Biosecurity, cleansing & disinfection of infected farms
 Number of susceptible animals
o Emergency vaccination or contiguous culling in severe situation.

Vesicular Stomatitis
Description:
A viral disease in the western hemisphere characterized by vesiculation, ulceration, and
erosion of oral/nasal mucosa, teats and coronary band which makes it clinically
indistinguishable from other vesicular diseases.
Etiology:
Vesiculovirus,
Family Rhabdoviridae
Transmission and Epidemiology
 Host:
o Common – Horse and Cattle and Pigs
o Less – Sheep and goats
o Humans – influenza like
o Calves – much resistant than adult cattle
 Vectors
o Biological vectors – Blackflies (Simulium vitattum)
o Mechanical Vectors – Sandflies
 o Mediate or immediate contagion
 Contact or ingestion of contaminated material, airborne, Convalescent
Cattle.
Pathogenesis, Clinical Finding/Lesions:
 Initial signs: fever, ptyalism
 Ulceration and erosions:
o No gross vesiculation due to immediate rupture
o Tongue and labial mucocutaneous junction
o Coronitis
o Teats and secondary mastitis
 Crusting
o Muzzle, udder, abdomen of horses.

Direct and Indirect contact, Vectors, Air

IP: 2-8 days

Hematogenous route

Primarily in the oral mucosa (less: foot and teat)

Self-limiting at 10-14 days

Diagnosis
 Virus isolation
o Fresh vesicular fluids and epithelial tissue like FMD
 Serological test:
o Competitive ELISA (faster and cheaper)
o Virus neutralization
o Compliment fixation
 PCR
 Clinical diagnosis:
o Indistinguishable from other Vesicular diseases
o VSV vs. FMD
 VSV less contagious
 VSV lesions generally found in one area of the body
 VSV has less morbidity
 VSV is self-limiting
Differential diagnosis of Vesicular and Ulcerative Viral disease

Cattle Swine Sheep Horses

FMD X X X
Swine Vesicular X
Disease
Vesicular x x x X
Stomatitis
Vesicular X
Exanthema of
swine
Rinderpest X
 IBR (Infectious X
Bovine
Rhinotracheitis)
BVD (Bovine X
Viral Diarrhea)
Malignant X
catarrhal fever
Bluetongue X X
Contagious X
Ecthyma

Treatment, control, and prevention

 No specific treatment
 Supportive (NSAID) / 2° bacterial infection (Antibiotic)
 Quarantine
 Movement control
 Insect control programs

Bluetongue
Sore muzzle, Pseudo Foot-and-mouth disease, Muzzle Dss.
Description:
A non-contagious insect-borne viral disease of ruminants
Etiology:
Orbivirus, Reoviridae (26 serotypes)
Transmission & Epidemiology:
 Primary host is sheep
 Subclinical: Cattle, goats, deer
 Geographic distribution: parallel with Culicoides spp. distribution. (Kung asa si colicoides
naa si Bluetongue didto)
 2-90% mortality
 High viral affinity to RBC (Invaginations in cell membrane safe from neutralizing
antibodies)
 Venereal transmission (semen)
 Transplacental (rare)
 Broad Band Distribution Worldwide
Pathogenesis
 Culicoides spp.
IP: 4-6 days

Endothelial damage (fever)

2 days after fever:

 Edema - Lips, nose, face, submandibular, eyelid, ears
 Congestion – Mouth, nose, nasal cavity, conjunctiva, coronary bands
 Hemorrhage, necrosis – where mechanical abrasions damage fragile arteries

Clinical finding/Lesion
 Sore muzzle – nose/nasal congestion
 Blue-tongue – swollen, protruding cyanotic tongue
 Serous to mucopurulent nasal secretions and crusting
 Ulceration – at the epithelial tissues in contact with the teeth
 Coronitis:
o Purple-red coronet
o Lameness
 Abortion and teratology
o Hydranencephaly
o Porencephaly
 Pulmonary artery – hemorrhages
 Papillary muscles – focal necrosis esp. at the left ventricle

Diagnosis
 Clinical diagnosis
 Virus isolation
o 10-20 ml blood at 4°C in anticoagulant
o Spleen, lymph, bone marrow
o Oxalate phenoglycerin – Long-term storage with no refrigeration
o If frozen – buffered lactose peptone at -70°C
o Embryonated chicken egg, Mammalian cell culture, insect cell culture
 PCR – for identification
 Serological tests:
o 7-14 days post-infection
o Competitive ELISA

Treatment, Control, and Prevention

  No specific treatment
 Supportive treatment
 Vaccination
o Inactivated and attenuated polyvalent vaccines (serial passage)
o Monovalent modified-live vaccine
o Never vaccinate during Culicoides season (High viral load during this season)
Modified live has the tendency to become live again / There could be an increase
in virulent or retain back its virulent.
 Insect control programs

Contagious Ecthyma
Orf, Contagious pustular dermatitis, Sore mouth
Description:
A zoonotic infectious dermatitis of small ruminants primarily affecting the lips of young
animals.
Etiology:
Parapoxvirus, Poxviridae
Transmission & Epidemiology
 Young sheep
 Worldwide
 Direct contact
 Environment stable
 Infected animals develop life-long immunity
Clinical finding/Lesions
 Primary lesion:
o Mucocutaneous junction of lips
o Gums of erupting incisor teeth
 Secondary Bacterial infections
o Strawberry foot rot – lesion on feet & coronary band w/ 2° Dermatophilus inf.
o Necrobacillosis – oral lesions with 2° Necrobacillus inf.
o Mastitis – teat of ewe’s lesions from infected lamb.
 Zoonosis – limited to face and hand
 Papules> Vesicles & pustules> encrustations> coalescence> large scabs> dermal tissue
proliferation> verrucose mass (scabs drop off) > Healing without scarring.
Diagnosis, Treatment, Control, and Prevention
 No specific treatment
 Supportive treatment
o Antibiotic against 2° bacterial infection
o Larvicide/repellant against myiasis
 Vaccination
o Live vaccine
o Brushed over tight skin scarification

Bovine Viral Diarrhea

“Mucosal Disease Complex”
Mycobacterial Disease in Ruminants
Tuberculosis (TB)
Description:
An endemic infectious granulomatous (chronic) zoonotic disease that practically affects
all vertebrate species
Epidemiology:

 All species are susceptible regardless of age

 Infected cattle are main source of infection but wildlife reservoir precludes eradication
 Inhalation is the major method of transmission
 Zebu are of less susceptibility
Difficult differential diagnosis because ruminant can make antibody out of M. avium complex.

Pathogenesis:
Inhalation of nasal droplets, ingestion via contaminated milk/water

Phagocytosis by alveolar macrophages (do/die)

Formation of primary foci

Purulent to caseous center may calcify

Granulation tissue surrounds forming a fibrous

capsule to form the classic tubercle

Primary foci similar lesions in the regional lymph node=Primary complex

Slow regression of the animal

 Primary complex in the base of the mesentery (movement of macrophages)
Clinical findings / lesion

 Bronchopneumonia – chronic, intermittent, moist cough, with later signs of dyspnea and
tachypnea (Ovine progressive adenocarcinoma, maedivisna)
 Ruminal tympany due to obstruction of the airways, gut and pharynx (lymph node
obstruction of esophagus in the mediastinum)
 Tuberculosis granuloma
 Progressive emaciation, lethargy, weakness, anorexia, low-grade fever (rare/lisud
makita kay halusa baka tambok kay nay surveillance)
 Lymph node enlargement
Infiltration of neutrophils, macrophages, epithelioid & mononucleated giant cells
SIGNS CORRELEATES TO THE SEVERITY OF LESIONS
Diagnosis

 Radiography
 Necropsy examination (demonstration of tuberculosis granuloma) High risk
 Isolation and identification (4-8wks culture).
 PCR (tracheal washes? / discharges)
 Direct smears stain with Ziehl-Neelsen (review diff. stain for diff bacteria)
 Intradermal tuberculin tests
o Single intradermal test (SID)
o Comparative tuberculin skin test
 Thermal test – pyrexia (>40°C) at 6-8 hrs. after SC inoculation (subjective)
 Stormont test – intradermal test followed 7 days after then read after 24 hrs. (Expensive
more specific)
Ancillary test:

 Lymphocyte proliferation and gammav interferon assays.

 ELISA
 False negative if animal is infected less than 30 days
If inconclusive give SID 1 week after previous SID. After 24 hrs. reread
Control and Prevention
Destruction
Limit the use of gluraldehyde and formaldehyde (carcinogenic)

Paratuberculosis
Johne’s dss, chronic wasting dss, granulomatous enteritis
Heinrich A. Johne
Description:
A chronic, contagious, granulomatous enteritis characterized in cattle by persistent
diarrhea, progressive weight loss, debilitation and eventually death.
Etiology:
Mycobacterium avium subs. Paratuberculosis
Epidemiology and transmission

 Worldwide
 Priority disease for international trade
 Highest published prevalence in dairy cattle
 Excreted in large number in feces
 Fecal-oral route
 Lower numbers in colostrum and milk
 Resistant to environmental factors
Tuberculosis in cattle can be transmitted via milk

 Killed by simple pasteurization for 60°C in 30 mins

Paratuberculosis are more resistant to environmental condition

Pathogenesis:

Malabsorptive diarrhea
Clinical findings/Lesions:

Protein-losing enteropathy is a differential of hemosep, blood parasite, hemocosis / hemoglosis?

Hypoproteinemia either johne’s or hemocosis (no protein in the blood)
Johne’s malabsorption of protein / hemocosis is due to blood sucking parasites
Loss of fats is due to ketosis

Signa may not correlate to the severity of the lesions

Diagnosis, Control and prevention.