NHP Bacterial Diseases

Question 0

What enteric pathogen is among the most common, and causes disease in marmosets, tamarins, macaques, baboons, apes, and humans. Significant dehydration is a key feature of clinical presentation. Results in a leukocytosis with a left shift.

Answer 0

Shigella spp. Shigella flexneri most frequently, including serotypes 1a, 2a, 3, 4, 5, 6, and 15.
S. sonnei and S. boydii occur less frequently.

(This could also potentially describe Campylobacter)

Question 1

Describe transmission of Shigella in NHPs.

Answer 1

Endemic infections maintained by asymptomatic carriers.

Infection and disease with antibody production do NOT provide immunity, and animals may be chronically reinfected.

Question 2

Describe typical clinical presentation of Shigella in NHPs.

Answer 2

Overt disease in endemic colonies may not manifest without a precipitating stressful event, such as social group disruption or transport.
Clinical signs typically foul-smelling, liquid stool with mucus, blood. Monkeys are weak and mod-severely dehydrated, needing prompt treatment. Severe localized gingivitis, abortion, and air sac infection can also occur.

Marmosets and tamarins do NOT show diarrhea as a primary sign, but are lethargic, depressed, and dehydrated with dried blood around anus.

Question 3

Describe typical gross lesions with Shigella in NHPs.

Answer 3

Occur primarily in cecum and colon. Colonic mucosa has fibrinopurulent exudate, and intestinal wall is edematous and hemorrhagic with focal ulceration.
May also see small intestine intususseption, rectal prolapse, splenomegaly, and mesenteric lymphadenopathy.

Gross lesions in marmosets and tamarins are confined to cecum and colon.

Question 4

What are the most frequent fecal bacterial isolates from subclinical and clinically affected NHPs?

Answer 4

Campylobacter jejuni, and C. coli

Question 5

How does prevalence of Campylobacter infection in macaques change over time?

Answer 5

Increases with time in captivity.

Question 6

How does Campylobacter usually present clinically?

Answer 6

Watery diarrhea, with mucohemorrhagic possible. WBC may be normal or may have leukocytosis with left shift. Severe electrolyte abnormalities: Na < 132, Cl < 93 mEq/L, with acidosis, and high anion gap.
Many infections are self-limiting.

Question 7

What is the antibiotic of choice for Campylobacter?

What other treatment is warranted?

Answer 7

Erythromycin historically, but resistance common so should be based on sensitivity if given at all.

Normonatremic fluids such as Lactated Ringers, or normal saline.

Question 8

What is the significance of isolating E. coli from a NHP fecal culture with diarrhea?

Answer 8

Questionable since its frequently isolated from clinically normal NHPs.

Enteropathogenic E. coli (EPEC) have been identified in rhesus monkeys with SIV.

Question 9

What are the most frequently reported serovars of Salmonella spp. In NHPs?

Answer 9

S. typhimurium, S. cholerasuis, S. anatum, S. stanley, S. derby, S. oranienburg

Question 10

What are the typical clinical signs of salmonellosis in NHPs?

Answer 10

Enteric forms can cause watery diarrhea, sometimes with hemorrhage or mucus; often with pyrexia

Extraintestinal signs include neonatal septicemia, abortion, osteomyelitis, pyelonephritis.

Question 11

What are the gross pathological signs of Salmonella?

Answer 11

Edema, hyperemia, and rare mucosal ulceration in ileum and colon. Enlargement of spleen and mesenteric lymph nodes may occur.

Question 12

How should Salmonella be treated in NHPs?

Answer 12

Antibiotic therapy should be reserved for those with severe diarrhea or septicemia to reduce chance of carrier state. Zoonotic potential and difficulty in eliminating carriers may necessitate culling carriers.

Other treatment involves supportive care to address fluid and electrolyte loss.

Question 13

What can cause fulminating enteric and systemic disease in marmosets, owl monkeys, squirrel monkeys, and Old World monkeys?

Answer 13

Yersinia enterocolitica, Y. Pseudotuberculosis

Question 14

How does yersiniosis typically present in NHPs?

Answer 14

Macaques: diarrhea, vomiting, severe abdominal pain, mild dehydration, blood-stained feces, abortions and stillbirths possible.

Squirrel monkeys: weak, inactive, enlarges cervical lymph nodes

Owl monkey: weakness, depression, diarrhea, abdominal distension, splenomegaly.

Question 15

What are the typical gross lesions with Yersinia infections in NHPs?

Answer 15

Multifocal hepatic and splenic necrosis or abscesses
Mesenteric lymphadenopathy
Ulcerative colitis

Squirrel monkeys are unique with cervical lymph node enlargement.

Question 16

How should Yersinia infections be treated?

Answer 16

Treatment is not usually attempted due to fulminating nature if disease.

Question 17

What clinical pathology signs usually accompany Yersinia infections in macaques? In owl monkeys?

Answer 17

Macaques: leukocytosis, hypo atresia, hypochloremia, prerenal azotemia, hyperfibrinogenemia

Owl monkeys: neutrophilia with left shift

Question 18

What are the clinical signs of Lawsonia intracellularis in macaques?

Answer 18

Mild or transient diarrhea, abdominal distension, or can be found dead with no clinical signs. Profound anemia (10% Hct).

Question 19

What is the most devastating respiratory pathogen in NHPs?

Answer 19

Streptococcus pneumoniae

Question 20

How is Strep. pneumoniae transmitted, and what are predisposing factors?

Answer 20

Transmitted by aerosol via the upper respiratory tract, middle ear, or mouth.
Stress-related factors predispose, such as capture, transport, quarantine, viral infection, waning passive immunity.

Question 21

What is the typical clinical presentation of Strep. pneumoniae in macaques?

Answer 21

Usually rapidly progressive. Death may occur within hours of onset of clinical signs.
Signs include panophthalmitis, conjunctivitis, lethargy, incoordination, hypothermia, depressed reflexes, ataxia, muscle tremors, head pressing, nuchal rigidity, nystagmus, leukocytosis with left shift.

Question 22

What is the typical clinical presentation of Strep. pneumoniae in chimpanzees?

Answer 22

Duration can range from 2-14 days. Sign initially URT with coughing, nasal discharge, followed by neurological signs.

Question 23

What provides a presumptive diagnosis of pneumococcal meningitis?

Answer 23

Free or phagocytized, encapsulated, Gram positive, diplococci in smears of CSF.

Question 24

What are the typical gross lesions of Strep. pneumoniae infection in macaques?

Answer 24

Engorgement of meningeal vasculature, thickening and opacification of leptomeninges, purulent exudate over cortex and ventricles. Lesions may extend to spinal cord.
In chronic disease, may see asymmetry of cerebral hemispheres and severe malaria of ventral frontal lobes.
Congestion of lungs, pulmonary edema, acute purulent bronchopneumonia, and gray hepatic action of ventral lung lobes.

Question 25

What characterizes S. pneumoniae infection microscopically?

Answer 25

Fibrinopurulent leptomeningitis extending into cerebral and cerebellar cortices.
(Fig. 13 on p. 736)

Question 26

What is the general clinical presentation and the range of susceptible NHP species for Klebsiella pneumoniae?

Answer 26

Pneumonia, meningitis, air sacculitis, septicemia, peritonitis, enteritis.
New and Old World monkeys, and apes.

Question 27

How is Klebsiella typically diagnosed?

Answer 27

Usually post-mortem. Ante-mortem diagnosis is difficult or impossible due to acute course of disease.
New World monkeys in particular may die from septicemia or peritonitis with no clinical signs.

Question 28

A _____ incidence of Klebsiella infection has been reported for tamarins, and ______ incidence for owl monkeys.

Answer 28

64%, 25-29%

Question 29

What gross lesions have been reported for callitrichids with Klebsiella infection?

Answer 29

Fibrinous lobar pneumonia, purulent peritonitis, mesenteric lymphadenopathy.

Question 30

What gross lesions in rhesus macaques have been reported with Klebsiella infection?

Answer 30

Exudative bronchopneumonia, hemopurulent meningitis

Question 31

How is Klebsiella treated?

Answer 31

Treatment difficult and not usually attempted due to fulminating course and high incidence if drug resistance.

Vaccination with autogenous vaccines in marmosets, owl monkeys, and squirrel monkeys is successful for prevention.

Question 32

What clinical signs are associated with Bordatella bronchiseptica in marmosets?

Answer 32

Bilateral mucopurulent nasal discharge, dyspnea during handling, pyrexia. Death resulted in some less than 1 year of age

Question 33

Which NHP species does Pasteurella multocida affect?

Answer 33

Primarily squirrel monkeys and owl monkeys. But, has also been reported on baboons secondary to surgical procedures, chair restraint, and chronic catheterization.

Question 34

How does Pasteurella multocida present in squirrel monkeys?

Answer 34

Unsteady gait, nystagmus, head tilt, circling.

Meningitis, otitis media, lymphadenitis, and myocarditis on necropsy.

Question 35

How does Pasteurella multocida present in owl monkeys?

Answer 35

Pneumonia, pleuritis, meningitis

Question 36

Describe Nocardia spp.

Answer 36

Aerobic actinomycete found in richly fertilized soil as saprophytes on decaying vegetation.
Nocardia asteroides is most common isolate in NHPs.

Question 37

How is Nocardia infection transmitted?

Answer 37

Contact with skin wounds, inhalation, or ingestion.

Question 38

How does Nocardia typically present?

Answer 38

Dyspnea, epistaxis, chronic weight loss, abdominal distension and discomfort, chronic intermittent diarrhea, lethargy, depression.

Radiographically, pulmonary lesions cannot be distinguished from tuberculosis.

Question 39

What are the gross lesions with Nocardia?

Answer 39

Pulmonary lesions include multinodular to diffuse red to gray areas of consolidation, pulmonary hemorrhage and edema, abscesses, and cavitary lesions.
Draining multinodular cutaneous lesions, or subcutaneous nodules are also possible.

Disseminated norcardiosis with multifocal abscesses in the momentum, mesentery, liver, kidney, and stomach, in addition to focal abscesses in the brain, has been reported in macaques.

Question 40

What are microscopic characteristics of Nocardia infection?

Answer 40

Multifocal to coalescing pyro granuloma containing sulfur granules with large colonies of filament outs bacteria. Multinucleated giant cells are found. At the periphery.

Question 41

How is Nocardia treated?

Answer 41

No reports of successful treatments.

Question 42

Epistaxis and sneezing in cynomolgus macaques?

Answer 42

Moraxella catarrhalis

Gram negative diplococcus

Question 43

Tuberculosis in NHPs is caused by what species?

Answer 43

Mycobacterium tuberculosis, M. bovis, M. africanum

Distribution and character of lesions is identical with all three.

Question 44

Gross lesions of tuberculosis in macaques?

Answer 44

Caseous nodules in hilar lymph nodes and lung, large cavitary and coalescing lesions in lung, and tubercles extending into thoracic pleura.
Can be secondary spread to spleen, kidney, liver, various lymph nodes.
Less frequently, tuberculous nodules are in cerebrum, spinal column, momentum, uterus, ovary, peripheral lymph nodes, skin, mammary gland, vertebrae.

Question 45

Typical microscopic lesions of tuberculosis?

Answer 45

Unencapsulated granulomas with necrotic core. Surrounding core are layers of epithelioid macrophages and lesser numbers of neutrophils, with multinucleate Langerhans’ giant cells at the periphery.
Mineralization is uncommon.
Acid Fast Bacilli can be demonstrated within lesions intra- and extracellularly.

Question 46

Describe the sensitivity and limitations of the tuberculin skin test.

Answer 46

Animals with early or advanced disease may give false negative reactions.
False negatives also can occur with:
1. Concomitant infection with measles virus due to immunosuppressive
2. Concomitant treatment with isoniazid

False positives possible with exposure to Freund’s complete adjuvant.

Question 47

Describe the diagnostic utility of thoracic radiographs for tuberculosis.

Answer 47

Can confirm pulmonary disease but cannot distinguish between tuberculosis, norcardiosis, and cryptococcosis.